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SOX4 Antibody (sample size)

CUT&Tag grade Abs

ChIP-seq grade Abs

ChIP grade Abs

Negative IgG control

Antibody portal

Antibodies

Catalog Number

Format

Price

C15310129-20

20 µl

$115.00
Bulk order

Other format

C15310129

100 µl

Alternative names: EVI16

Polyclonal antibody raised in rabbit against human SOX4 (SRY (sex determining region Y)-box 4), using two KLH-conjugated synthetic peptides containing a sequence from the N-terminus and from the C-terminus of the protein, respectively.

Lot	A574-004
Concentration	Not determined
Species reactivity	Human, mouse: positive. Other species: not tested.
Type	Polyclonal
Purity	Whole antiserum
Host	Rabbit
Storage Conditions	Store at -20°C; for long storage, store at -80°C. Avoid multiple freeze-thaw cycles.
Storage Buffer	Whole antiserum from rabbit containing 0.05% azide.
Precautions	This product is for research use only. Not for use in diagnostic or therapeutic procedures.

Applications	Suggested dilution	References
ELISA	1:100 - 1:1,000	Fig 1
Western Blotting	1:4,000	Fig 2, 3
IP	6 µl/IP	Fig 4

Validation data

Figure 1. Determination of the titer
To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.

Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4
A. H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 µg) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.
B. Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.

Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4
Western blot was performed on Protein extracts (~40 µg) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA.

Figure 4. IP using the Diagenode antibody directed against SOX4
IP was performed overnight on protein extracts (600 µg) from CT-2A (A) and GL261 (B) cells using 6 µl of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1.

Publications

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MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functionsin hepatocellular carcinoma by directly targeting hepatoma-derived growthfactor HDGF.
Huge Nicole et al.
BACKGROUND: In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigen...

Differential Expression of Members of SOX Family of Transcription Factorsin Failing Human Hearts
Chia-Feng, Liu and Ying, Ng and Varun, Thachil and Michael, Morley andChristine, S Moravec and W., H. Wilson Tang
Background: The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays essential roles during development and in many disease processes. Several SOX proteins, e.g., SOX4, SOX11, and SOX9, are required for normal heart morphogenesis. SOX9 was shown to contribute to...

Global analysis of histone modifications and long-range chromatin interactions revealed the differential cistrome changes and novel transcriptional players in human dilated cardiomyopathy.
Liu CF, Abnousi A, Bazeley P, Ni Y, Morley M, Moravec CS, Hu M, Tang WHW
BACKGROUND: Acetylation and methylation of histones alter the chromatin structure and accessibility that affect transcriptional regulators binding to enhancers and promoters. The binding of transcriptional regulators enables the interaction between enhancers and promoters, thus affecting gene expression. However, ou...

SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis.
Vervoort SJ, Lourenço AR, Tufegdzic Vidakovic A, Mocholi E, Sandoval JL, Rueda OM, Frederiks C, Pals C, Peeters JGC, Caldas C, Bruna A, Coffer PJ
Expression of the transcription factor SOX4 is often elevated in human cancers, where it generally correlates with tumor-progression and poor-disease outcome. Reduction of SOX4 expression results in both diminished tumor-incidence and metastasis. In breast cancer, TGF-β-mediated induction of SOX4 has been shown...

SOX4 inhibits oligodendrocyte differentiation of embryonic neural stem cells in vitro by inducing Hes5 expression
Braccioli Luca, Vervoort Stephin J., Puma Gianmarco, Nijboer Cora H., Coffer Paul J.
SOX4 has been shown to promote neuronal differentiation both in the adult and embryonic neural progenitors. Ectopic SOX4 expression has also been shown to inhibit oligodendrocyte differentiation in mice, however the underlying molecular mechanisms remain poorly understood. Here we demonstrate that SOX4 regulates tra...

TRPM7 controls mesenchymal features of breast cancer cells by tensional regulation of SOX4.
Kuipers AJ, Middelbeek J, Vrenken K, Pérez-González C, Poelmans G, Klarenbeek J, Jalink K, Trepat X, van Leeuwen FN
Mechanically induced signaling pathways are important drivers of tumor progression. However, if and how mechanical signals affect metastasis or therapy response remains poorly understood. We previously found that the channel-kinase TRPM7, a regulator of cellular tension implicated in mechano-sensory processes, is re...

Cancer cell specific inhibition of Wnt/β-catenin signaling by forced intracellular acidification.
Melnik S, Dvornikov D, Müller-Decker K, Depner S, Stannek P, Meister M, Warth A, Thomas M, Muley T, Risch A, Plass C, Klingmüller U, Niehrs C, Glinka A
Use of the diabetes type II drug Metformin is associated with a moderately lowered risk of cancer incidence in numerous tumor entities. Studying the molecular changes associated with the tumor-suppressive action of Metformin we found that the oncogene , which is upregulated in solid tumors and associated with poor p...

Sox4 Expression Confers Bladder Cancer Stem Cell Properties and Predicts for Poor Patient Outcome
Shen H et al.
Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). We have previously found that amplification of chromosome 6p22 is significantly associated with the muscle-invasive rather than superficial...

Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.
Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M
The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ab...

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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
</div>
</div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig3.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
</div>
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<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig4.jpg" alt="IP" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
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<li><strong>Focused</strong> -&nbsp;Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
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<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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			'description' => '<p><span style="font-weight: 400;">The list of Diagenode&rsquo;s highly specific antibodies for transcription studies includes the antibodies against many transcription factors and nuclear receptors. &nbsp;Check the list below to see our targets.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 100% satisfaction guarantee</span></li>
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			'meta_keywords' => ' Transcription factor antibodies,monoclonal antibodies,polyclonal antibodies',
			'meta_description' => 'Diagenode offers polyclonal and monoclonal antibodies for Transcription studie',
			'meta_title' => 'Transcription factor Antibodies | Diagenode',
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			'name' => 'All antibodies',
			'description' => '<p><span style="font-weight: 400;">All Diagenode&rsquo;s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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			'meta_description' => 'Diagenode Offers Strict quality standards with Rigorous QC and validated Antibodies. Classified based on level of validation for flexibility of Application. Comprehensive selection of histone and non-histone Antibodies',
			'meta_title' => 'Diagenode's selection of Antibodies is exclusively dedicated for Epigenetic Research | Diagenode',
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			'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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			'alt' => 'Mouse IgG',
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			'id' => '4439',
			'name' => 'MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functionsin hepatocellular carcinoma by directly targeting hepatoma-derived growthfactor HDGF.',
			'authors' => 'Huge  Nicole et al.',
			'description' => '<p>BACKGROUND: In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis. METHODS: Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined. RESULTS: HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3'UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs. CONCLUSIONS: This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis.</p>',
			'date' => '2022-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35578240',
			'doi' => '10.1186/s12935-022-02582-2',
			'modified' => '2022-09-28 09:28:36',
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		(int) 1 => array(
			'id' => '4014',
			'name' => 'Differential Expression of Members of SOX Family of Transcription Factorsin Failing Human Hearts',
			'authors' => 'Chia-Feng, Liu and Ying, Ng and Varun, Thachil and Michael, Morley andChristine, S Moravec and W., H. Wilson Tang',
			'description' => '<p>Background: The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays essential roles during development and in many disease processes. Several SOX proteins, e.g., SOX4, SOX11, and SOX9, are required for normal heart morphogenesis. SOX9 was shown to contribute to cardiac fibrosis in animal models. However, differential expression of other SOX transcription factors and their functional roles in the failing human myocardium have not been explored. Methods and Findings: All 20 SOX genes from RNA-seq data were extracted, and their RNA levels were compared to the NF, DCM, and hypertrophic cardiomyopathy (HCM) groups. The protein levels of the differential expressed SOX genes were confirmed by Western blot. Four SOX genes whose RNA levels were significantly upregulated in DCM or HCM compared to NF. However, only SOX4 and SOX8 proteins were markedly increased in the heart failure groups. Gene co-expression network analysis identified genes associated and respond similarly to perturbations with SOX4 in cardiac tissues. Using a meta-analysis combining epigenetics and genome-wide association data, we reported several genomic variants associated with HF phenotype linked to SOX4 or SOX8. Conclusions: Elevation of SOX8 and SOX4 are observed in the failing human myocardium. The molecular mechanism associated with them in HF warrants further investigation.</p>',
			'date' => '2020-08-19',
			'pmid' => 'https://www.researchsquare.com/article/rs-52488/v1',
			'doi' => 'https://doi.org/10.21203/rs.3.rs-52488/v1',
			'modified' => '2020-12-16 17:33:59',
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		),
		(int) 2 => array(
			'id' => '3970',
			'name' => 'Global analysis of histone modifications and long-range chromatin interactions revealed the differential cistrome changes and novel transcriptional players in human dilated cardiomyopathy.',
			'authors' => 'Liu CF, Abnousi A, Bazeley P, Ni Y, Morley M, Moravec CS, Hu M, Tang WHW',
			'description' => '<p>BACKGROUND: Acetylation and methylation of histones alter the chromatin structure and accessibility that affect transcriptional regulators binding to enhancers and promoters. The binding of transcriptional regulators enables the interaction between enhancers and promoters, thus affecting gene expression. However, our knowledge of these epigenetic alternations in patients with heart failure remains limited. METHODS AND RESULTS: From the comprehensive analysis of major histone modifications, 3-dimensional chromatin interactions, and transcriptome in left ventricular (LV) tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors, differential active enhancer and promoter regions were identified between NF and DCM. Moreover, the genome-wide average promoter signal is significantly lower in DCM than in NF. Super-enhancer (SE) analysis revealed that fewer SEs were found in DCM LVs than in NF ones, and three unique SE-associated genes between NF and DCM were identified. Moreover, SEs are enriched within the genomic region associated with long-range chromatin interactions. The differential enhancer-promoter interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. CONCLUSIONS: We have established the cistrome of four histone modifications and chromatin interactome for enhancers and promoters in NF and DCM tissues. Differential histone modifications and enhancer-promoter interactions were found in DCM, which were associated with gene expression levels of a subset of disease-associated genes in human heart failure.</p>',
			'date' => '2020-06-10',
			'pmid' => 'http://www.pubmed.gov/32533974',
			'doi' => '10.1016/j.yjmcc.2020.06.001',
			'modified' => '2020-08-12 09:30:21',
			'created' => '2020-08-10 12:12:25',
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		(int) 3 => array(
			'id' => '3414',
			'name' => 'SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis.',
			'authors' => 'Vervoort SJ, Lourenço AR, Tufegdzic Vidakovic A, Mocholi E, Sandoval JL, Rueda OM, Frederiks C, Pals C, Peeters JGC, Caldas C, Bruna A, Coffer PJ',
			'description' => '<p>Expression of the transcription factor SOX4 is often elevated in human cancers, where it generally correlates with tumor-progression and poor-disease outcome. Reduction of SOX4 expression results in both diminished tumor-incidence and metastasis. In breast cancer, TGF-&beta;-mediated induction of SOX4 has been shown to contribute to epithelial-to-mesenchymal transition (EMT), which controls pro-metastatic events. Here, we identify SMAD3 as a novel, functionally relevant SOX4 interaction partner. Genome-wide analysis showed that SOX4 and SMAD3 co-occupy a large number of genomic loci in a cell-type specific manner. Moreover, SOX4 expression was required for TGF-&beta;-mediated induction of a subset of SMAD3/SOX4-co-bound genes regulating migration and extracellular matrix-associated processes, and correlating with poor-prognosis. These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-&beta;. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-&beta; signaling, thereby impairing tumorigenesis.</p>',
			'date' => '2018-10-12',
			'pmid' => 'http://www.pubmed.gov/30137431',
			'doi' => '10.1093/nar/gky755',
			'modified' => '2018-12-31 11:20:11',
			'created' => '2018-12-04 09:51:07',
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			'id' => '3397',
			'name' => 'SOX4 inhibits oligodendrocyte differentiation of embryonic neural stem cells in vitro by inducing Hes5 expression',
			'authors' => 'Braccioli Luca, Vervoort Stephin J., Puma Gianmarco, Nijboer Cora H., Coffer Paul J.',
			'description' => '<p>SOX4 has been shown to promote neuronal differentiation both in the adult and embryonic neural progenitors. Ectopic SOX4 expression has also been shown to inhibit oligodendrocyte differentiation in mice, however the underlying molecular mechanisms remain poorly understood. Here we demonstrate that SOX4 regulates transcriptional targets associated with neural development in neural stem cells (NSCs), reducing the expression of genes promoting oligodendrocyte differentiation. Interestingly, we observe that SOX4 levels decreased during oligodendrocyte differentiation in vitro. Moreover, we show that SOX4 knockdown induces increased oligodendrocyte differentiation, as the percentage of Olig2- positive/2',3'-Cyclic-nucleotide 3'-phosphodiesterase (CNPase)-positive maturing oligodendrocytes increases, while the number of Olig2-positive oligodendrocyte precursors is unaffected. Conversely, conditional SOX4 overexpression utilizing a doxycycline inducible system decreases the percentage of maturing oligodendrocytes, suggesting that SOX4 inhibits maturation from precursor to mature oligodendrocyte. We identify the transcription factor Hes5 as a direct SOX4 target gene and we show that conditional overexpression of Hes5 rescues the increased oligodendrocyte differentiation mediated by SOX4 depletion in NSCs. Taken together, these observations support a novel role for SOX4 in NSC by controlling oligodendrocyte differentiation through induction of Hes5 expression.</p>',
			'date' => '2018-10-04',
			'pmid' => 'http://www.pubmed.gov/30343100',
			'doi' => '10.1016/j.scr.2018.10.005',
			'modified' => '2018-11-09 11:52:20',
			'created' => '2018-11-08 12:59:45',
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		(int) 5 => array(
			'id' => '3424',
			'name' => 'TRPM7 controls mesenchymal features of breast cancer cells by tensional regulation of SOX4.',
			'authors' => 'Kuipers AJ, Middelbeek J, Vrenken K, Pérez-González C, Poelmans G, Klarenbeek J, Jalink K, Trepat X, van Leeuwen FN',
			'description' => '<p>Mechanically induced signaling pathways are important drivers of tumor progression. However, if and how mechanical signals affect metastasis or therapy response remains poorly understood. We previously found that the channel-kinase TRPM7, a regulator of cellular tension implicated in mechano-sensory processes, is required for breast cancer metastasis in vitro and in vivo. Here, we show that TRPM7 contributes to maintaining a mesenchymal phenotype in breast cancer cells by tensional regulation of the EMT transcription factor SOX4. The functional consequences of SOX4 knockdown closely mirror those produced by TRPM7 knockdown. By traction force measurements, we demonstrate that TRPM7 reduces cytoskeletal tension through inhibition of myosin II activity. Moreover, we show that SOX4 expression and downstream mesenchymal markers are inversely regulated by cytoskeletal tension and matrix rigidity. Overall, our results identify SOX4 as a transcription factor that is uniquely sensitive to cellular tension and indicate that TRPM7 may contribute to breast cancer progression by tensional regulation of SOX4.</p>',
			'date' => '2018-07-01',
			'pmid' => 'http://www.pubmed.gov/29684587',
			'doi' => '10.1016/j.bbadis.2018.04.017',
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			'authors' => 'Melnik S, Dvornikov D, Müller-Decker K, Depner S, Stannek P, Meister M, Warth A, Thomas M, Muley T, Risch A, Plass C, Klingmüller U, Niehrs C, Glinka A',
			'description' => '<p>Use of the diabetes type II drug Metformin is associated with a moderately lowered risk of cancer incidence in numerous tumor entities. Studying the molecular changes associated with the tumor-suppressive action of Metformin we found that the oncogene , which is upregulated in solid tumors and associated with poor prognosis, was induced by Wnt/&beta;-catenin signaling and blocked by Metformin. Wnt signaling inhibition by Metformin was surprisingly specific for cancer cells. Unraveling the underlying specificity, we identified Metformin and other Mitochondrial Complex I (MCI) inhibitors as inducers of intracellular acidification in cancer cells. We demonstrated that acidification triggers the unfolded protein response to induce the global transcriptional repressor , known to block Wnt signaling. Moreover, our results suggest that intracellular acidification universally inhibits Wnt signaling. Based on these findings, we combined MCI inhibitors with H ionophores, to escalate cancer cells into intracellular hyper-acidification and ATP depletion. This treatment lowered intracellular pH both in vitro and in a mouse xenograft tumor model, depleted cellular ATP, blocked Wnt signaling, downregulated , and strongly decreased stemness and viability of cancer cells. Importantly, the inhibition of Wnt signaling occurred downstream of &beta;-catenin, encouraging applications in treatment of cancers caused by and mutations.</p>',
			'date' => '2018-01-01',
			'pmid' => 'http://www.pubmed.gov/29977599',
			'doi' => '10.1038/s41421-018-0033-2',
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			'authors' => 'Shen H et al.',
			'description' => '<p>Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). We have previously found that amplification of chromosome 6p22 is significantly associated with the muscle-invasive rather than superficial TCC-UB. Here, we demonstrated that Sox4, one of the candidate oncogenes located within the chromosome 6p22 amplicon, confers bladder cancer stem cell (CSC) properties. Down-regulation of Sox4 led to the inhibition of cell migration, colony formation as well as mesenchymal-to-epithelial transition (MET). Interestingly, knockdown of Sox4 also reduced the sphere formation, enriched cell population with high levels of aldehyde dehydrogenase (ALDH (high)) and tumor formation potential. Using gene expression profiling, we further identified novel Sox4 target genes. Last, immunohistochemistry analysis of human bladder tumor tissue microarrays (TMAs) indicated that high Sox4 expression was correlated with advanced cancer stages and poor survival rate. In summary, our data show that Sox4 is an important regulator of the bladder CSC properties and it may serve as a biomarker of the aggressive phenotype in bladder cancer.</p>',
			'date' => '2015-11-01',
			'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26681916',
			'doi' => ' 10.7150/ijbs.13240',
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			'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
			'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
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<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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	'position' => '10',
	'parent_id' => '40',
	'name' => 'ELISA',
	'description' => '<div class="row">
<div class="small-12 medium-12 large-12 columns">Enzyme-linked immunosorbent assay.</div>
</div>',
	'in_footer' => false,
	'in_menu' => false,
	'online' => true,
	'tabular' => true,
	'slug' => 'elisa-antibodies',
	'meta_keywords' => ' ELISA Antibodies,Monoclonal antibody, Polyclonal antibody',
	'meta_description' => 'Diagenode offers Monoclonal & Polyclonal antibodies for ELISA applications',
	'meta_title' => 'ELISA Antibodies - Monoclonal & Polyclonal antibody | Diagenode',
	'modified' => '2016-01-13 12:21:41',
	'created' => '2014-07-08 08:13:28',
	'ProductsApplication' => array(
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		'product_id' => '3051',
		'application_id' => '20'
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)
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	(int) 0 => 'elisa-antibodies'
)
$applications = array(
	'id' => '20',
	'position' => '10',
	'parent_id' => '40',
	'name' => 'ELISA',
	'description' => '<div class="row">
<div class="small-12 medium-12 large-12 columns">Enzyme-linked immunosorbent assay.</div>
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	'in_footer' => false,
	'in_menu' => false,
	'online' => true,
	'tabular' => true,
	'slug' => 'elisa-antibodies',
	'meta_keywords' => ' ELISA Antibodies,Monoclonal antibody, Polyclonal antibody',
	'meta_description' => 'Diagenode offers Monoclonal & Polyclonal antibodies for ELISA applications',
	'meta_title' => 'ELISA Antibodies - Monoclonal & Polyclonal antibody | Diagenode',
	'modified' => '2016-01-13 12:21:41',
	'created' => '2014-07-08 08:13:28',
	'locale' => 'eng'
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$description = '<div class="row">
<div class="small-12 medium-12 large-12 columns">Enzyme-linked immunosorbent assay.</div>
</div>'
$name = 'ELISA'
$document = array(
	'id' => '671',
	'name' => 'Datasheet SOX4 CS-129-100',
	'description' => 'Datasheet description',
	'image_id' => null,
	'type' => 'Datasheet',
	'url' => 'files/products/antibodies/Datasheet_SOX4_CS-129-100.pdf',
	'slug' => 'datasheet-sox4-cs-129-100',
	'meta_keywords' => null,
	'meta_description' => null,
	'modified' => '2015-07-07 11:47:44',
	'created' => '2015-07-07 11:47:44',
	'ProductsDocument' => array(
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		'product_id' => '3051',
		'document_id' => '671'
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$sds = array(
	'id' => '2972',
	'name' => 'SOX4 antibody SDS ES es',
	'language' => 'es',
	'url' => 'files/SDS/SOX4/SDS-C15310129-SOX4_antibody-ES-es-GHS_1_0.pdf',
	'countries' => 'ES',
	'modified' => '2023-01-10 13:37:52',
	'created' => '2023-01-10 13:37:52',
	'ProductsSafetySheet' => array(
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		'product_id' => '3051',
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$publication = array(
	'id' => '687',
	'name' => 'Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.',
	'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
	'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
	'date' => '2012-01-01',
	'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22084397',
	'doi' => '',
	'modified' => '2015-07-24 15:38:58',
	'created' => '2015-07-24 15:38:58',
	'ProductsPublication' => array(
		'id' => '4230',
		'product_id' => '3051',
		'publication_id' => '687'
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)
$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/22084397" target="_blank"><i class="fa fa-external-link"></i></a>'
include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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<div id="request_formModal" class="reveal-modal medium" data-reveal aria-labelledby="modalTitle" aria-hidden="true" role="dialog">
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$viewFile = '/home/website-server/www/app/View/Products/view.ctp'
$dataForView = array(
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	'meta_keywords' => '',
	'meta_description' => 'SOX4 (SRY (sex determining region Y)-box 4) Polyclonal Antibody  validated  in  WB and ELISA.  Batch-specific data available on the website. Alternative names: EVI16',
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			'antibody_id' => '306',
			'name' => 'SOX4 Antibody (sample size)',
			'description' => '',
			'label1' => 'Validation data',
			'info1' => '',
			'label2' => '',
			'info2' => '',
			'label3' => '',
			'info3' => '',
			'format' => '20 µl',
			'catalog_number' => 'C15310129-20',
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			'price_USD' => '115',
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			'slug' => 'sox4-polyclonal-antibody-pioneer-20-ul',
			'meta_title' => 'SOX4 Polyclonal Antibody (sample size) | Diagenode',
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			'created' => '2020-01-27 12:04:58',
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<thead>
<tr>
<th>Applications</th>
<th>Suggested dilution</th>
<th>References</th>
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<tbody>
<tr>
<td>ELISA</td>
<td>1:100 - 1:1,000</td>
<td>Fig 1</td>
</tr>
<tr>
<td>Western Blotting</td>
<td>1:4,000</td>
<td>Fig 2, 3</td>
</tr>
<tr>
<td>IP</td>
<td>6 &micro;l/IP</td>
<td>Fig 4</td>
</tr>
</tbody>
</table>
<p></p>',
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			'precautions' => 'This product is for research use only. Not for use in diagnostic or therapeutic procedures.',
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			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2020-04-23 13:27:35',
			'created' => '0000-00-00 00:00:00',
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$meta_keywords = ''
$meta_description = 'SOX4 (SRY (sex determining region Y)-box 4) Polyclonal Antibody  validated  in  WB and ELISA.  Batch-specific data available on the website. Alternative names: EVI16'
$meta_title = 'SOX4 Polyclonal Antibody (sample size) | Diagenode'
$product = array(
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		'antibody_id' => '306',
		'name' => 'SOX4 Antibody (sample size)',
		'description' => '<p><span>Alternative names: <strong>EVI16</strong></span></p>
<p><span>Polyclonal antibody raised in rabbit against human SOX4 (SRY (sex determining region Y)-box 4), using two KLH-conjugated synthetic peptides containing a sequence from the N-terminus and from the C-terminus of the protein, respectively.</span></p>',
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		'info1' => '<div class="row">
<div class="small-5 columns">
<p><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig1.jpg" alt="ELISA" style="display: block; margin-left: auto; margin-right: auto;" /><br /><br /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
</div>
</div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig2.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
</div>
</div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig3.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
</div>
</div>
<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig4.jpg" alt="IP" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
</div>
</div>',
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		'info3' => '',
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		'slug' => 'sox4-polyclonal-antibody-pioneer-20-ul',
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		'clonality' => '',
		'isotype' => '',
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		'concentration' => 'Not determined',
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		'type' => 'Polyclonal',
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		'classification' => 'Pioneer',
		'application_table' => '<table>
<thead>
<tr>
<th>Applications</th>
<th>Suggested dilution</th>
<th>References</th>
</tr>
</thead>
<tbody>
<tr>
<td>ELISA</td>
<td>1:100 - 1:1,000</td>
<td>Fig 1</td>
</tr>
<tr>
<td>Western Blotting</td>
<td>1:4,000</td>
<td>Fig 2, 3</td>
</tr>
<tr>
<td>IP</td>
<td>6 &micro;l/IP</td>
<td>Fig 4</td>
</tr>
</tbody>
</table>
<p></p>',
		'storage_conditions' => 'Store at -20°C; for long storage, store at -80°C. Avoid multiple freeze-thaw cycles.',
		'storage_buffer' => 'Whole antiserum from rabbit containing 0.05% azide.',
		'precautions' => 'This product is for research use only. Not for use in diagnostic or therapeutic procedures.',
		'uniprot_acc' => '',
		'slug' => '',
		'meta_keywords' => '',
		'meta_description' => '',
		'modified' => '2020-04-23 13:27:35',
		'created' => '0000-00-00 00:00:00',
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			'antibody_id' => '306',
			'name' => 'SOX4 Antibody',
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<p><span>Polyclonal antibody raised in rabbit against human SOX4 (SRY (sex determining region Y)-box 4), using two KLH-conjugated synthetic peptides containing a sequence from the N-terminus and from the C-terminus of the protein, respectively.</span></p>',
			'label1' => 'Validation data',
			'info1' => '<div class="row">
<div class="small-5 columns">
<p><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig1.jpg" alt="ELISA" style="display: block; margin-left: auto; margin-right: auto;" /><br /><br /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
</div>
</div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig2.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
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<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig3.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
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<div class="small-7 columns">
<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
</div>
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<div class="extra-spaced"></div>
<div class="extra-spaced"></div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig4.jpg" alt="IP" style="display: block; margin-left: auto; margin-right: auto;" /></p>
</div>
<div class="small-7 columns">
<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
<ul>
<li><strong>Focused</strong> -&nbsp;Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
</ul>
<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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			'description' => '<p><span style="font-weight: 400;">The list of Diagenode&rsquo;s highly specific antibodies for transcription studies includes the antibodies against many transcription factors and nuclear receptors. &nbsp;Check the list below to see our targets.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 100% satisfaction guarantee</span></li>
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			'meta_keywords' => ' Transcription factor antibodies,monoclonal antibodies,polyclonal antibodies',
			'meta_description' => 'Diagenode offers polyclonal and monoclonal antibodies for Transcription studie',
			'meta_title' => 'Transcription factor Antibodies | Diagenode',
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			'name' => 'All antibodies',
			'description' => '<p><span style="font-weight: 400;">All Diagenode&rsquo;s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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			'meta_description' => 'Diagenode Offers Strict quality standards with Rigorous QC and validated Antibodies. Classified based on level of validation for flexibility of Application. Comprehensive selection of histone and non-histone Antibodies',
			'meta_title' => 'Diagenode's selection of Antibodies is exclusively dedicated for Epigenetic Research | Diagenode',
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			'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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			'description' => '<p>More than in any other immuoprecipitation assays, quality antibodies are critical tools in many epigenetics experiments. Since 10 years, Diagenode has developed the most stringent quality production available on the market for antibodies exclusively focused on epigenetic uses. All our antibodies have been qualified to work in epigenetic applications.</p>',
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			'name' => 'Datasheet SOX4 CS-129-100',
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			'url' => 'files/products/antibodies/Datasheet_SOX4_CS-129-100.pdf',
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			'alt' => 'Mouse IgG',
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			'id' => '4439',
			'name' => 'MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functionsin hepatocellular carcinoma by directly targeting hepatoma-derived growthfactor HDGF.',
			'authors' => 'Huge  Nicole et al.',
			'description' => '<p>BACKGROUND: In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis. METHODS: Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined. RESULTS: HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3'UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs. CONCLUSIONS: This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis.</p>',
			'date' => '2022-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35578240',
			'doi' => '10.1186/s12935-022-02582-2',
			'modified' => '2022-09-28 09:28:36',
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		),
		(int) 1 => array(
			'id' => '4014',
			'name' => 'Differential Expression of Members of SOX Family of Transcription Factorsin Failing Human Hearts',
			'authors' => 'Chia-Feng, Liu and Ying, Ng and Varun, Thachil and Michael, Morley andChristine, S Moravec and W., H. Wilson Tang',
			'description' => '<p>Background: The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays essential roles during development and in many disease processes. Several SOX proteins, e.g., SOX4, SOX11, and SOX9, are required for normal heart morphogenesis. SOX9 was shown to contribute to cardiac fibrosis in animal models. However, differential expression of other SOX transcription factors and their functional roles in the failing human myocardium have not been explored. Methods and Findings: All 20 SOX genes from RNA-seq data were extracted, and their RNA levels were compared to the NF, DCM, and hypertrophic cardiomyopathy (HCM) groups. The protein levels of the differential expressed SOX genes were confirmed by Western blot. Four SOX genes whose RNA levels were significantly upregulated in DCM or HCM compared to NF. However, only SOX4 and SOX8 proteins were markedly increased in the heart failure groups. Gene co-expression network analysis identified genes associated and respond similarly to perturbations with SOX4 in cardiac tissues. Using a meta-analysis combining epigenetics and genome-wide association data, we reported several genomic variants associated with HF phenotype linked to SOX4 or SOX8. Conclusions: Elevation of SOX8 and SOX4 are observed in the failing human myocardium. The molecular mechanism associated with them in HF warrants further investigation.</p>',
			'date' => '2020-08-19',
			'pmid' => 'https://www.researchsquare.com/article/rs-52488/v1',
			'doi' => 'https://doi.org/10.21203/rs.3.rs-52488/v1',
			'modified' => '2020-12-16 17:33:59',
			'created' => '2020-10-12 14:54:59',
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		),
		(int) 2 => array(
			'id' => '3970',
			'name' => 'Global analysis of histone modifications and long-range chromatin interactions revealed the differential cistrome changes and novel transcriptional players in human dilated cardiomyopathy.',
			'authors' => 'Liu CF, Abnousi A, Bazeley P, Ni Y, Morley M, Moravec CS, Hu M, Tang WHW',
			'description' => '<p>BACKGROUND: Acetylation and methylation of histones alter the chromatin structure and accessibility that affect transcriptional regulators binding to enhancers and promoters. The binding of transcriptional regulators enables the interaction between enhancers and promoters, thus affecting gene expression. However, our knowledge of these epigenetic alternations in patients with heart failure remains limited. METHODS AND RESULTS: From the comprehensive analysis of major histone modifications, 3-dimensional chromatin interactions, and transcriptome in left ventricular (LV) tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors, differential active enhancer and promoter regions were identified between NF and DCM. Moreover, the genome-wide average promoter signal is significantly lower in DCM than in NF. Super-enhancer (SE) analysis revealed that fewer SEs were found in DCM LVs than in NF ones, and three unique SE-associated genes between NF and DCM were identified. Moreover, SEs are enriched within the genomic region associated with long-range chromatin interactions. The differential enhancer-promoter interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. CONCLUSIONS: We have established the cistrome of four histone modifications and chromatin interactome for enhancers and promoters in NF and DCM tissues. Differential histone modifications and enhancer-promoter interactions were found in DCM, which were associated with gene expression levels of a subset of disease-associated genes in human heart failure.</p>',
			'date' => '2020-06-10',
			'pmid' => 'http://www.pubmed.gov/32533974',
			'doi' => '10.1016/j.yjmcc.2020.06.001',
			'modified' => '2020-08-12 09:30:21',
			'created' => '2020-08-10 12:12:25',
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		),
		(int) 3 => array(
			'id' => '3414',
			'name' => 'SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis.',
			'authors' => 'Vervoort SJ, Lourenço AR, Tufegdzic Vidakovic A, Mocholi E, Sandoval JL, Rueda OM, Frederiks C, Pals C, Peeters JGC, Caldas C, Bruna A, Coffer PJ',
			'description' => '<p>Expression of the transcription factor SOX4 is often elevated in human cancers, where it generally correlates with tumor-progression and poor-disease outcome. Reduction of SOX4 expression results in both diminished tumor-incidence and metastasis. In breast cancer, TGF-&beta;-mediated induction of SOX4 has been shown to contribute to epithelial-to-mesenchymal transition (EMT), which controls pro-metastatic events. Here, we identify SMAD3 as a novel, functionally relevant SOX4 interaction partner. Genome-wide analysis showed that SOX4 and SMAD3 co-occupy a large number of genomic loci in a cell-type specific manner. Moreover, SOX4 expression was required for TGF-&beta;-mediated induction of a subset of SMAD3/SOX4-co-bound genes regulating migration and extracellular matrix-associated processes, and correlating with poor-prognosis. These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-&beta;. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-&beta; signaling, thereby impairing tumorigenesis.</p>',
			'date' => '2018-10-12',
			'pmid' => 'http://www.pubmed.gov/30137431',
			'doi' => '10.1093/nar/gky755',
			'modified' => '2018-12-31 11:20:11',
			'created' => '2018-12-04 09:51:07',
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		(int) 4 => array(
			'id' => '3397',
			'name' => 'SOX4 inhibits oligodendrocyte differentiation of embryonic neural stem cells in vitro by inducing Hes5 expression',
			'authors' => 'Braccioli Luca, Vervoort Stephin J., Puma Gianmarco, Nijboer Cora H., Coffer Paul J.',
			'description' => '<p>SOX4 has been shown to promote neuronal differentiation both in the adult and embryonic neural progenitors. Ectopic SOX4 expression has also been shown to inhibit oligodendrocyte differentiation in mice, however the underlying molecular mechanisms remain poorly understood. Here we demonstrate that SOX4 regulates transcriptional targets associated with neural development in neural stem cells (NSCs), reducing the expression of genes promoting oligodendrocyte differentiation. Interestingly, we observe that SOX4 levels decreased during oligodendrocyte differentiation in vitro. Moreover, we show that SOX4 knockdown induces increased oligodendrocyte differentiation, as the percentage of Olig2- positive/2',3'-Cyclic-nucleotide 3'-phosphodiesterase (CNPase)-positive maturing oligodendrocytes increases, while the number of Olig2-positive oligodendrocyte precursors is unaffected. Conversely, conditional SOX4 overexpression utilizing a doxycycline inducible system decreases the percentage of maturing oligodendrocytes, suggesting that SOX4 inhibits maturation from precursor to mature oligodendrocyte. We identify the transcription factor Hes5 as a direct SOX4 target gene and we show that conditional overexpression of Hes5 rescues the increased oligodendrocyte differentiation mediated by SOX4 depletion in NSCs. Taken together, these observations support a novel role for SOX4 in NSC by controlling oligodendrocyte differentiation through induction of Hes5 expression.</p>',
			'date' => '2018-10-04',
			'pmid' => 'http://www.pubmed.gov/30343100',
			'doi' => '10.1016/j.scr.2018.10.005',
			'modified' => '2018-11-09 11:52:20',
			'created' => '2018-11-08 12:59:45',
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		),
		(int) 5 => array(
			'id' => '3424',
			'name' => 'TRPM7 controls mesenchymal features of breast cancer cells by tensional regulation of SOX4.',
			'authors' => 'Kuipers AJ, Middelbeek J, Vrenken K, Pérez-González C, Poelmans G, Klarenbeek J, Jalink K, Trepat X, van Leeuwen FN',
			'description' => '<p>Mechanically induced signaling pathways are important drivers of tumor progression. However, if and how mechanical signals affect metastasis or therapy response remains poorly understood. We previously found that the channel-kinase TRPM7, a regulator of cellular tension implicated in mechano-sensory processes, is required for breast cancer metastasis in vitro and in vivo. Here, we show that TRPM7 contributes to maintaining a mesenchymal phenotype in breast cancer cells by tensional regulation of the EMT transcription factor SOX4. The functional consequences of SOX4 knockdown closely mirror those produced by TRPM7 knockdown. By traction force measurements, we demonstrate that TRPM7 reduces cytoskeletal tension through inhibition of myosin II activity. Moreover, we show that SOX4 expression and downstream mesenchymal markers are inversely regulated by cytoskeletal tension and matrix rigidity. Overall, our results identify SOX4 as a transcription factor that is uniquely sensitive to cellular tension and indicate that TRPM7 may contribute to breast cancer progression by tensional regulation of SOX4.</p>',
			'date' => '2018-07-01',
			'pmid' => 'http://www.pubmed.gov/29684587',
			'doi' => '10.1016/j.bbadis.2018.04.017',
			'modified' => '2018-12-31 11:38:35',
			'created' => '2018-12-04 09:51:07',
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		),
		(int) 6 => array(
			'id' => '3452',
			'name' => 'Cancer cell specific inhibition of Wnt/β-catenin signaling by forced intracellular acidification.',
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			'description' => '<p>Use of the diabetes type II drug Metformin is associated with a moderately lowered risk of cancer incidence in numerous tumor entities. Studying the molecular changes associated with the tumor-suppressive action of Metformin we found that the oncogene , which is upregulated in solid tumors and associated with poor prognosis, was induced by Wnt/&beta;-catenin signaling and blocked by Metformin. Wnt signaling inhibition by Metformin was surprisingly specific for cancer cells. Unraveling the underlying specificity, we identified Metformin and other Mitochondrial Complex I (MCI) inhibitors as inducers of intracellular acidification in cancer cells. We demonstrated that acidification triggers the unfolded protein response to induce the global transcriptional repressor , known to block Wnt signaling. Moreover, our results suggest that intracellular acidification universally inhibits Wnt signaling. Based on these findings, we combined MCI inhibitors with H ionophores, to escalate cancer cells into intracellular hyper-acidification and ATP depletion. This treatment lowered intracellular pH both in vitro and in a mouse xenograft tumor model, depleted cellular ATP, blocked Wnt signaling, downregulated , and strongly decreased stemness and viability of cancer cells. Importantly, the inhibition of Wnt signaling occurred downstream of &beta;-catenin, encouraging applications in treatment of cancers caused by and mutations.</p>',
			'date' => '2018-01-01',
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			'doi' => '10.1038/s41421-018-0033-2',
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			'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
			'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
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<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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	'name' => 'Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.',
	'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
	'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
	'date' => '2012-01-01',
	'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22084397',
	'doi' => '',
	'modified' => '2015-07-24 15:38:58',
	'created' => '2015-07-24 15:38:58',
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$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/22084397" target="_blank"><i class="fa fa-external-link"></i></a>'
include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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<td>Fig 2, 3</td>
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<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig4.jpg" alt="IP" style="display: block; margin-left: auto; margin-right: auto;" /></p>
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<div class="small-7 columns">
<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<th>Suggested dilution</th>
<th>References</th>
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<td>Fig 1</td>
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<tr>
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<td>Fig 2, 3</td>
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<div class="small-5 columns">
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<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
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</div>
<div class="row">
<div class="small-5 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig2.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
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<div class="small-7 columns">
<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against SOX4<br />A.</strong> H1299 lung carcinoma cells were transfected with HA-tagged SOX4 (lane 1) or with a HA-tagged truncated SOX4 (395X mutant, lane 2). Whole cell extracts (60 - 100 &micro;g) were analysed by Western blot using the Diagenode antibody against SOX4 (Cat. No. C15310129) diluted 1:4,000 in TBS-Tween containing 2% skimmed milk. The position of the protein of interest is indicated on the right; the marker (in kDa) is shown on the left.<br /> <strong>B.</strong> Whole cell extracts of 4 different lung carcinoma cell lines were analysed by Western blot with the Diagenode antibody against SOX4 as described above. The H522 cells are known to overexpress SOX4. Western blot performed by Montse Sanchez-Cespedes and Sandra Castillo Diez, Catalan Institute of Oncology, Barcelona, Spain.</small></p>
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<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310129_fig3.jpg" alt="Western blot" style="display: block; margin-left: auto; margin-right: auto;" /></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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			'price_EUR' => '260',
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			'price_JPY' => '40730',
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			'meta_title' => 'SOX4 Polyclonal Antibody | Diagenode',
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			'meta_description' => 'SOX4 (SRY (sex determining region Y)-box 4) Polyclonal Antibody  validated  in  WB and ELISA.  Batch-specific data available on the website. Alternative names: EVI16',
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			'description' => '<p><strong>Western blot</strong> : The quality of antibodies used in this technique is crucial for correct and specific protein identification. Diagenode offers huge selection of highly sensitive and specific western blot-validated antibodies.</p>
<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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			'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for western blot applications',
			'meta_title' => ' Western Blot  - Monoclonal antibody - Polyclonal antibody  | Diagenode',
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<div class="small-12 medium-12 large-12 columns">Enzyme-linked immunosorbent assay.</div>
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			'meta_keywords' => ' ELISA Antibodies,Monoclonal antibody, Polyclonal antibody',
			'meta_description' => 'Diagenode offers Monoclonal & Polyclonal antibodies for ELISA applications',
			'meta_title' => 'ELISA Antibodies - Monoclonal & Polyclonal antibody | Diagenode',
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			'name' => 'Sample size antibodies',
			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
<ul>
<li><strong>Focused</strong> -&nbsp;Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
</ul>
<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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			'meta_keywords' => '5-hmC monoclonal antibody,CRISPR/Cas9 polyclonal antibody ,H3K36me3 polyclonal antibody,diagenode',
			'meta_description' => 'Diagenode offers sample volume on selected antibodies for researchers to test, validate and provide confidence and flexibility in choosing from our wide range of antibodies ',
			'meta_title' => 'Sample-size Antibodies | Diagenode',
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			'name' => 'Transcription',
			'description' => '<p><span style="font-weight: 400;">The list of Diagenode&rsquo;s highly specific antibodies for transcription studies includes the antibodies against many transcription factors and nuclear receptors. &nbsp;Check the list below to see our targets.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 100% satisfaction guarantee</span></li>
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			'meta_keywords' => ' Transcription factor antibodies,monoclonal antibodies,polyclonal antibodies',
			'meta_description' => 'Diagenode offers polyclonal and monoclonal antibodies for Transcription studie',
			'meta_title' => 'Transcription factor Antibodies | Diagenode',
			'modified' => '2020-07-06 12:59:19',
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			'name' => 'All antibodies',
			'description' => '<p><span style="font-weight: 400;">All Diagenode&rsquo;s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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			'meta_description' => 'Diagenode Offers Strict quality standards with Rigorous QC and validated Antibodies. Classified based on level of validation for flexibility of Application. Comprehensive selection of histone and non-histone Antibodies',
			'meta_title' => 'Diagenode's selection of Antibodies is exclusively dedicated for Epigenetic Research | Diagenode',
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			'name' => 'Antibodies you can trust',
			'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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			'url' => 'files/posters/Antibodies_you_can_trust_Poster.pdf',
			'slug' => 'antibodies-you-can-trust-poster',
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			'modified' => '2015-10-01 20:18:31',
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			'id' => '38',
			'name' => 'Epigenetic Antibodies Brochure',
			'description' => '<p>More than in any other immuoprecipitation assays, quality antibodies are critical tools in many epigenetics experiments. Since 10 years, Diagenode has developed the most stringent quality production available on the market for antibodies exclusively focused on epigenetic uses. All our antibodies have been qualified to work in epigenetic applications.</p>',
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			'type' => 'Brochure',
			'url' => 'files/brochures/Epigenetic_Antibodies_Brochure.pdf',
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			'name' => 'Datasheet SOX4 CS-129-100',
			'description' => 'Datasheet description',
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			'type' => 'Datasheet',
			'url' => 'files/products/antibodies/Datasheet_SOX4_CS-129-100.pdf',
			'slug' => 'datasheet-sox4-cs-129-100',
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			'alt' => 'Mouse IgG',
			'modified' => '2020-11-27 07:00:09',
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			'id' => '4439',
			'name' => 'MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functionsin hepatocellular carcinoma by directly targeting hepatoma-derived growthfactor HDGF.',
			'authors' => 'Huge  Nicole et al.',
			'description' => '<p>BACKGROUND: In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis. METHODS: Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined. RESULTS: HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3'UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs. CONCLUSIONS: This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis.</p>',
			'date' => '2022-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35578240',
			'doi' => '10.1186/s12935-022-02582-2',
			'modified' => '2022-09-28 09:28:36',
			'created' => '2022-09-08 16:32:20',
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		(int) 1 => array(
			'id' => '4014',
			'name' => 'Differential Expression of Members of SOX Family of Transcription Factorsin Failing Human Hearts',
			'authors' => 'Chia-Feng, Liu and Ying, Ng and Varun, Thachil and Michael, Morley andChristine, S Moravec and W., H. Wilson Tang',
			'description' => '<p>Background: The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays essential roles during development and in many disease processes. Several SOX proteins, e.g., SOX4, SOX11, and SOX9, are required for normal heart morphogenesis. SOX9 was shown to contribute to cardiac fibrosis in animal models. However, differential expression of other SOX transcription factors and their functional roles in the failing human myocardium have not been explored. Methods and Findings: All 20 SOX genes from RNA-seq data were extracted, and their RNA levels were compared to the NF, DCM, and hypertrophic cardiomyopathy (HCM) groups. The protein levels of the differential expressed SOX genes were confirmed by Western blot. Four SOX genes whose RNA levels were significantly upregulated in DCM or HCM compared to NF. However, only SOX4 and SOX8 proteins were markedly increased in the heart failure groups. Gene co-expression network analysis identified genes associated and respond similarly to perturbations with SOX4 in cardiac tissues. Using a meta-analysis combining epigenetics and genome-wide association data, we reported several genomic variants associated with HF phenotype linked to SOX4 or SOX8. Conclusions: Elevation of SOX8 and SOX4 are observed in the failing human myocardium. The molecular mechanism associated with them in HF warrants further investigation.</p>',
			'date' => '2020-08-19',
			'pmid' => 'https://www.researchsquare.com/article/rs-52488/v1',
			'doi' => 'https://doi.org/10.21203/rs.3.rs-52488/v1',
			'modified' => '2020-12-16 17:33:59',
			'created' => '2020-10-12 14:54:59',
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		),
		(int) 2 => array(
			'id' => '3970',
			'name' => 'Global analysis of histone modifications and long-range chromatin interactions revealed the differential cistrome changes and novel transcriptional players in human dilated cardiomyopathy.',
			'authors' => 'Liu CF, Abnousi A, Bazeley P, Ni Y, Morley M, Moravec CS, Hu M, Tang WHW',
			'description' => '<p>BACKGROUND: Acetylation and methylation of histones alter the chromatin structure and accessibility that affect transcriptional regulators binding to enhancers and promoters. The binding of transcriptional regulators enables the interaction between enhancers and promoters, thus affecting gene expression. However, our knowledge of these epigenetic alternations in patients with heart failure remains limited. METHODS AND RESULTS: From the comprehensive analysis of major histone modifications, 3-dimensional chromatin interactions, and transcriptome in left ventricular (LV) tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors, differential active enhancer and promoter regions were identified between NF and DCM. Moreover, the genome-wide average promoter signal is significantly lower in DCM than in NF. Super-enhancer (SE) analysis revealed that fewer SEs were found in DCM LVs than in NF ones, and three unique SE-associated genes between NF and DCM were identified. Moreover, SEs are enriched within the genomic region associated with long-range chromatin interactions. The differential enhancer-promoter interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. CONCLUSIONS: We have established the cistrome of four histone modifications and chromatin interactome for enhancers and promoters in NF and DCM tissues. Differential histone modifications and enhancer-promoter interactions were found in DCM, which were associated with gene expression levels of a subset of disease-associated genes in human heart failure.</p>',
			'date' => '2020-06-10',
			'pmid' => 'http://www.pubmed.gov/32533974',
			'doi' => '10.1016/j.yjmcc.2020.06.001',
			'modified' => '2020-08-12 09:30:21',
			'created' => '2020-08-10 12:12:25',
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		),
		(int) 3 => array(
			'id' => '3414',
			'name' => 'SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis.',
			'authors' => 'Vervoort SJ, Lourenço AR, Tufegdzic Vidakovic A, Mocholi E, Sandoval JL, Rueda OM, Frederiks C, Pals C, Peeters JGC, Caldas C, Bruna A, Coffer PJ',
			'description' => '<p>Expression of the transcription factor SOX4 is often elevated in human cancers, where it generally correlates with tumor-progression and poor-disease outcome. Reduction of SOX4 expression results in both diminished tumor-incidence and metastasis. In breast cancer, TGF-&beta;-mediated induction of SOX4 has been shown to contribute to epithelial-to-mesenchymal transition (EMT), which controls pro-metastatic events. Here, we identify SMAD3 as a novel, functionally relevant SOX4 interaction partner. Genome-wide analysis showed that SOX4 and SMAD3 co-occupy a large number of genomic loci in a cell-type specific manner. Moreover, SOX4 expression was required for TGF-&beta;-mediated induction of a subset of SMAD3/SOX4-co-bound genes regulating migration and extracellular matrix-associated processes, and correlating with poor-prognosis. These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-&beta;. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-&beta; signaling, thereby impairing tumorigenesis.</p>',
			'date' => '2018-10-12',
			'pmid' => 'http://www.pubmed.gov/30137431',
			'doi' => '10.1093/nar/gky755',
			'modified' => '2018-12-31 11:20:11',
			'created' => '2018-12-04 09:51:07',
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		(int) 4 => array(
			'id' => '3397',
			'name' => 'SOX4 inhibits oligodendrocyte differentiation of embryonic neural stem cells in vitro by inducing Hes5 expression',
			'authors' => 'Braccioli Luca, Vervoort Stephin J., Puma Gianmarco, Nijboer Cora H., Coffer Paul J.',
			'description' => '<p>SOX4 has been shown to promote neuronal differentiation both in the adult and embryonic neural progenitors. Ectopic SOX4 expression has also been shown to inhibit oligodendrocyte differentiation in mice, however the underlying molecular mechanisms remain poorly understood. Here we demonstrate that SOX4 regulates transcriptional targets associated with neural development in neural stem cells (NSCs), reducing the expression of genes promoting oligodendrocyte differentiation. Interestingly, we observe that SOX4 levels decreased during oligodendrocyte differentiation in vitro. Moreover, we show that SOX4 knockdown induces increased oligodendrocyte differentiation, as the percentage of Olig2- positive/2',3'-Cyclic-nucleotide 3'-phosphodiesterase (CNPase)-positive maturing oligodendrocytes increases, while the number of Olig2-positive oligodendrocyte precursors is unaffected. Conversely, conditional SOX4 overexpression utilizing a doxycycline inducible system decreases the percentage of maturing oligodendrocytes, suggesting that SOX4 inhibits maturation from precursor to mature oligodendrocyte. We identify the transcription factor Hes5 as a direct SOX4 target gene and we show that conditional overexpression of Hes5 rescues the increased oligodendrocyte differentiation mediated by SOX4 depletion in NSCs. Taken together, these observations support a novel role for SOX4 in NSC by controlling oligodendrocyte differentiation through induction of Hes5 expression.</p>',
			'date' => '2018-10-04',
			'pmid' => 'http://www.pubmed.gov/30343100',
			'doi' => '10.1016/j.scr.2018.10.005',
			'modified' => '2018-11-09 11:52:20',
			'created' => '2018-11-08 12:59:45',
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		),
		(int) 5 => array(
			'id' => '3424',
			'name' => 'TRPM7 controls mesenchymal features of breast cancer cells by tensional regulation of SOX4.',
			'authors' => 'Kuipers AJ, Middelbeek J, Vrenken K, Pérez-González C, Poelmans G, Klarenbeek J, Jalink K, Trepat X, van Leeuwen FN',
			'description' => '<p>Mechanically induced signaling pathways are important drivers of tumor progression. However, if and how mechanical signals affect metastasis or therapy response remains poorly understood. We previously found that the channel-kinase TRPM7, a regulator of cellular tension implicated in mechano-sensory processes, is required for breast cancer metastasis in vitro and in vivo. Here, we show that TRPM7 contributes to maintaining a mesenchymal phenotype in breast cancer cells by tensional regulation of the EMT transcription factor SOX4. The functional consequences of SOX4 knockdown closely mirror those produced by TRPM7 knockdown. By traction force measurements, we demonstrate that TRPM7 reduces cytoskeletal tension through inhibition of myosin II activity. Moreover, we show that SOX4 expression and downstream mesenchymal markers are inversely regulated by cytoskeletal tension and matrix rigidity. Overall, our results identify SOX4 as a transcription factor that is uniquely sensitive to cellular tension and indicate that TRPM7 may contribute to breast cancer progression by tensional regulation of SOX4.</p>',
			'date' => '2018-07-01',
			'pmid' => 'http://www.pubmed.gov/29684587',
			'doi' => '10.1016/j.bbadis.2018.04.017',
			'modified' => '2018-12-31 11:38:35',
			'created' => '2018-12-04 09:51:07',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '3452',
			'name' => 'Cancer cell specific inhibition of Wnt/β-catenin signaling by forced intracellular acidification.',
			'authors' => 'Melnik S, Dvornikov D, Müller-Decker K, Depner S, Stannek P, Meister M, Warth A, Thomas M, Muley T, Risch A, Plass C, Klingmüller U, Niehrs C, Glinka A',
			'description' => '<p>Use of the diabetes type II drug Metformin is associated with a moderately lowered risk of cancer incidence in numerous tumor entities. Studying the molecular changes associated with the tumor-suppressive action of Metformin we found that the oncogene , which is upregulated in solid tumors and associated with poor prognosis, was induced by Wnt/&beta;-catenin signaling and blocked by Metformin. Wnt signaling inhibition by Metformin was surprisingly specific for cancer cells. Unraveling the underlying specificity, we identified Metformin and other Mitochondrial Complex I (MCI) inhibitors as inducers of intracellular acidification in cancer cells. We demonstrated that acidification triggers the unfolded protein response to induce the global transcriptional repressor , known to block Wnt signaling. Moreover, our results suggest that intracellular acidification universally inhibits Wnt signaling. Based on these findings, we combined MCI inhibitors with H ionophores, to escalate cancer cells into intracellular hyper-acidification and ATP depletion. This treatment lowered intracellular pH both in vitro and in a mouse xenograft tumor model, depleted cellular ATP, blocked Wnt signaling, downregulated , and strongly decreased stemness and viability of cancer cells. Importantly, the inhibition of Wnt signaling occurred downstream of &beta;-catenin, encouraging applications in treatment of cancers caused by and mutations.</p>',
			'date' => '2018-01-01',
			'pmid' => 'http://www.pubmed.gov/29977599',
			'doi' => '10.1038/s41421-018-0033-2',
			'modified' => '2019-02-15 21:43:46',
			'created' => '2019-02-14 15:01:22',
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		(int) 7 => array(
			'id' => '2936',
			'name' => 'Sox4 Expression Confers Bladder Cancer Stem Cell Properties and Predicts for Poor Patient Outcome',
			'authors' => 'Shen H et al.',
			'description' => '<p>Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). We have previously found that amplification of chromosome 6p22 is significantly associated with the muscle-invasive rather than superficial TCC-UB. Here, we demonstrated that Sox4, one of the candidate oncogenes located within the chromosome 6p22 amplicon, confers bladder cancer stem cell (CSC) properties. Down-regulation of Sox4 led to the inhibition of cell migration, colony formation as well as mesenchymal-to-epithelial transition (MET). Interestingly, knockdown of Sox4 also reduced the sphere formation, enriched cell population with high levels of aldehyde dehydrogenase (ALDH (high)) and tumor formation potential. Using gene expression profiling, we further identified novel Sox4 target genes. Last, immunohistochemistry analysis of human bladder tumor tissue microarrays (TMAs) indicated that high Sox4 expression was correlated with advanced cancer stages and poor survival rate. In summary, our data show that Sox4 is an important regulator of the bladder CSC properties and it may serve as a biomarker of the aggressive phenotype in bladder cancer.</p>',
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			'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26681916',
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			'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
			'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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	'countries' => 'ES',
	'modified' => '2023-01-10 13:37:52',
	'created' => '2023-01-10 13:37:52',
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$publication = array(
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	'name' => 'Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.',
	'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
	'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
	'date' => '2012-01-01',
	'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22084397',
	'doi' => '',
	'modified' => '2015-07-24 15:38:58',
	'created' => '2015-07-24 15:38:58',
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$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/22084397" target="_blank"><i class="fa fa-external-link"></i></a>'
include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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<p><small><strong>Figure 4. IP using the Diagenode antibody directed against SOX4<br /></strong>IP was performed overnight on protein extracts (600 &micro;g) from CT-2A (A) and GL261 (B) cells using 6 &micro;l of the Diagenode antibody against SOX4 (Cat. No. C15310129). The immunoprecipitated proteins were subsequently analysed by Western blot with the antibody as described above. Lane 2 shows the result of the IP; the input is shown in lane 1. </small></p>
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<p><small><strong>Figure 1. Determination of the titer</strong><br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against human SOX4 (Cat. No. C15310129). The plates were coated with the peptides used for immunization of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:18,000.</small></p>
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<p><small><strong>Figure 3. Western blot analysis using the Diagenode antibody directed against SOX4<br /></strong>Western blot was performed on Protein extracts (~40 &micro;g) from mouse B16-OVA (A), CT-2A (B), GL261 (C) or B16A (D) cells using the Diagenode antibody against SOX4 (Cat. No. C15310129). The cells were transfected with a SOX4 specific crRNA (lanes 2) or with a negative control crRNA (lanes 1). The antibody was diluted 1:4,000 in TBS-Tween containing 5% skimmed milk. The position of the protein of interest is indicated on the right. The lower panel shows the WB results with a GAPDH antibody used as loading control. Western blot performed by Anže Godicelj, Dana Farber Cancer Institute, Boston, USA. </small></p>
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			'description' => '<p><strong>Western blot</strong> : The quality of antibodies used in this technique is crucial for correct and specific protein identification. Diagenode offers huge selection of highly sensitive and specific western blot-validated antibodies.</p>
<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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			'meta_description' => 'Diagenode offers a wide range of antibodies and technical support for western blot applications',
			'meta_title' => ' Western Blot  - Monoclonal antibody - Polyclonal antibody  | Diagenode',
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			'name' => 'ELISA',
			'description' => '<div class="row">
<div class="small-12 medium-12 large-12 columns">Enzyme-linked immunosorbent assay.</div>
</div>',
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			'slug' => 'elisa-antibodies',
			'meta_keywords' => ' ELISA Antibodies,Monoclonal antibody, Polyclonal antibody',
			'meta_description' => 'Diagenode offers Monoclonal & Polyclonal antibodies for ELISA applications',
			'meta_title' => 'ELISA Antibodies - Monoclonal & Polyclonal antibody | Diagenode',
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			'created' => '2014-07-08 08:13:28',
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			'id' => '102',
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			'name' => 'Sample size antibodies',
			'description' => '<h1><strong>Validated epigenetics antibodies</strong>&nbsp;&ndash; care for a sample?<br />&nbsp;</h1>
<p>Diagenode has partnered with leading epigenetics experts and numerous epigenetics consortiums to bring to you a validated and comprehensive collection of epigenetic antibodies. As an expert in epigenetics, we are committed to offering highly-specific antibodies validated for ChIP/ChIP-seq and many other applications. All batch-specific validation data is available on our website.<br /><a href="../categories/antibodies">Read about our expertise in antibody production</a>.</p>
<ul>
<li><strong>Focused</strong> -&nbsp;Diagenode's selection of antibodies is exclusively dedicated for epigenetic research. <a title="See the full collection." href="../categories/all-antibodies">See the full collection.</a></li>
<li><strong>Strict quality standards</strong>&nbsp;with rigorous QC and validation</li>
<li><strong>Classified</strong>&nbsp;based on level of validation for flexibility of application</li>
</ul>
<p>Existing sample sizes are listed below. We will soon expand our collection. &nbsp;Are you looking for a sample size of another antibody? Just <a href="mailto:agnieszka.zelisko@diagenode.com?Subject=Sample%20Size%20Request" target="_top">Contact us</a>.</p>',
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			'slug' => 'sample-size-antibodies',
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			'meta_keywords' => '5-hmC monoclonal antibody,CRISPR/Cas9 polyclonal antibody ,H3K36me3 polyclonal antibody,diagenode',
			'meta_description' => 'Diagenode offers sample volume on selected antibodies for researchers to test, validate and provide confidence and flexibility in choosing from our wide range of antibodies ',
			'meta_title' => 'Sample-size Antibodies | Diagenode',
			'modified' => '2019-07-03 10:57:05',
			'created' => '2015-10-27 12:13:34',
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			'position' => '50',
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			'name' => 'Transcription',
			'description' => '<p><span style="font-weight: 400;">The list of Diagenode&rsquo;s highly specific antibodies for transcription studies includes the antibodies against many transcription factors and nuclear receptors. &nbsp;Check the list below to see our targets.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; Highly sensitive and specific</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Cost-effective (requires less antibody per reaction)</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Batch-specific data is available on the website</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Expert technical support</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;Sample sizes available</span></li>
<li><span style="font-weight: 400;"> &nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp; 100% satisfaction guarantee</span></li>
</ul>',
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			'slug' => 'transcription-factor',
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			'meta_keywords' => ' Transcription factor antibodies,monoclonal antibodies,polyclonal antibodies',
			'meta_description' => 'Diagenode offers polyclonal and monoclonal antibodies for Transcription studie',
			'meta_title' => 'Transcription factor Antibodies | Diagenode',
			'modified' => '2020-07-06 12:59:19',
			'created' => '2015-03-12 10:20:08',
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			'id' => '103',
			'position' => '0',
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			'name' => 'All antibodies',
			'description' => '<p><span style="font-weight: 400;">All Diagenode&rsquo;s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
</ul>',
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			'slug' => 'all-antibodies',
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			'meta_keywords' => 'Antibodies,Premium Antibodies,Classic,Pioneer',
			'meta_description' => 'Diagenode Offers Strict quality standards with Rigorous QC and validated Antibodies. Classified based on level of validation for flexibility of Application. Comprehensive selection of histone and non-histone Antibodies',
			'meta_title' => 'Diagenode's selection of Antibodies is exclusively dedicated for Epigenetic Research | Diagenode',
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			'created' => '2015-11-02 14:49:22',
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			'id' => '11',
			'name' => 'Antibodies you can trust',
			'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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			'type' => 'Poster',
			'url' => 'files/posters/Antibodies_you_can_trust_Poster.pdf',
			'slug' => 'antibodies-you-can-trust-poster',
			'meta_keywords' => '',
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			'modified' => '2015-10-01 20:18:31',
			'created' => '2015-07-03 16:05:15',
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		(int) 1 => array(
			'id' => '38',
			'name' => 'Epigenetic Antibodies Brochure',
			'description' => '<p>More than in any other immuoprecipitation assays, quality antibodies are critical tools in many epigenetics experiments. Since 10 years, Diagenode has developed the most stringent quality production available on the market for antibodies exclusively focused on epigenetic uses. All our antibodies have been qualified to work in epigenetic applications.</p>',
			'image_id' => null,
			'type' => 'Brochure',
			'url' => 'files/brochures/Epigenetic_Antibodies_Brochure.pdf',
			'slug' => 'epigenetic-antibodies-brochure',
			'meta_keywords' => '',
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			'id' => '671',
			'name' => 'Datasheet SOX4 CS-129-100',
			'description' => 'Datasheet description',
			'image_id' => null,
			'type' => 'Datasheet',
			'url' => 'files/products/antibodies/Datasheet_SOX4_CS-129-100.pdf',
			'slug' => 'datasheet-sox4-cs-129-100',
			'meta_keywords' => null,
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			'id' => '250',
			'name' => 'product/antibodies/antibody.png',
			'alt' => 'Mouse IgG',
			'modified' => '2020-11-27 07:00:09',
			'created' => '2015-07-17 10:12:18',
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			'id' => '4439',
			'name' => 'MiR-129-5p exerts Wnt signaling-dependent tumor-suppressive functionsin hepatocellular carcinoma by directly targeting hepatoma-derived growthfactor HDGF.',
			'authors' => 'Huge  Nicole et al.',
			'description' => '<p>BACKGROUND: In hepatocellular carcinoma (HCC), histone deacetylases (HDACs) are frequently overexpressed. This results in chromatin compaction and silencing of tumor-relevant genes and microRNAs. Modulation of microRNA expression is a potential treatment option for HCC. Therefore, we aimed to characterize the epigenetically regulated miR-129-5p regarding its functional effects and target genes to understand its relevance for HCC tumorigenesis. METHODS: Global miRNA expression of HCC cell lines (HLE, HLF, Huh7, HepG2, Hep3B) and normal liver cell lines (THLE-2, THLE-3) was analyzed after HDAC inhibition by miRNA sequencing. An in vivo xenograft mouse model and in vitro assays were used to investigate tumor-relevant functional effects following miR-129-5p transfection of HCC cells. To validate hepatoma-derived growth factor (HDGF) as a direct target gene of miR-129-5p, luciferase reporter assays were performed. Survival data and HDGF expression were analyzed in public HCC datasets. After siRNA-mediated knockdown of HDGF, its cancer-related functions were examined. RESULTS: HDAC inhibition induced the expression of miR-129-5p. Transfection of miR-129-5p increased the apoptosis of HCC cells, decreased proliferation, migration and ERK signaling in vitro and inhibited tumor growth in vivo. Direct binding of miR-129-5p to the 3'UTR of HDGF via a noncanonical binding site was validated by luciferase reporter assays. HDGF knockdown reduced cell viability and migration and increased apoptosis in Wnt-inactive HCC cells. These in vitro results were in line with the analysis of public HCC datasets showing that HDGF overexpression correlated with a worse survival prognosis, primarily in Wnt-inactive HCCs. CONCLUSIONS: This study provides detailed insights into the regulatory network of the tumor-suppressive, epigenetically regulated miR-129-5p in HCC. Our results reveal for the first time that the therapeutic application of mir-129-5p may have significant implications for the personalized treatment of patients with Wnt-inactive, advanced HCC by directly regulating HDGF. Therefore, miR-129-5p is a promising candidate for a microRNA replacement therapy to prevent HCC progression and tumor metastasis.</p>',
			'date' => '2022-05-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/35578240',
			'doi' => '10.1186/s12935-022-02582-2',
			'modified' => '2022-09-28 09:28:36',
			'created' => '2022-09-08 16:32:20',
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			)
		),
		(int) 1 => array(
			'id' => '4014',
			'name' => 'Differential Expression of Members of SOX Family of Transcription Factorsin Failing Human Hearts',
			'authors' => 'Chia-Feng, Liu and Ying, Ng and Varun, Thachil and Michael, Morley andChristine, S Moravec and W., H. Wilson Tang',
			'description' => '<p>Background: The Sry-related high-mobility-group box (SOX) gene family, with 20 known transcription factors in humans, plays essential roles during development and in many disease processes. Several SOX proteins, e.g., SOX4, SOX11, and SOX9, are required for normal heart morphogenesis. SOX9 was shown to contribute to cardiac fibrosis in animal models. However, differential expression of other SOX transcription factors and their functional roles in the failing human myocardium have not been explored. Methods and Findings: All 20 SOX genes from RNA-seq data were extracted, and their RNA levels were compared to the NF, DCM, and hypertrophic cardiomyopathy (HCM) groups. The protein levels of the differential expressed SOX genes were confirmed by Western blot. Four SOX genes whose RNA levels were significantly upregulated in DCM or HCM compared to NF. However, only SOX4 and SOX8 proteins were markedly increased in the heart failure groups. Gene co-expression network analysis identified genes associated and respond similarly to perturbations with SOX4 in cardiac tissues. Using a meta-analysis combining epigenetics and genome-wide association data, we reported several genomic variants associated with HF phenotype linked to SOX4 or SOX8. Conclusions: Elevation of SOX8 and SOX4 are observed in the failing human myocardium. The molecular mechanism associated with them in HF warrants further investigation.</p>',
			'date' => '2020-08-19',
			'pmid' => 'https://www.researchsquare.com/article/rs-52488/v1',
			'doi' => 'https://doi.org/10.21203/rs.3.rs-52488/v1',
			'modified' => '2020-12-16 17:33:59',
			'created' => '2020-10-12 14:54:59',
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			)
		),
		(int) 2 => array(
			'id' => '3970',
			'name' => 'Global analysis of histone modifications and long-range chromatin interactions revealed the differential cistrome changes and novel transcriptional players in human dilated cardiomyopathy.',
			'authors' => 'Liu CF, Abnousi A, Bazeley P, Ni Y, Morley M, Moravec CS, Hu M, Tang WHW',
			'description' => '<p>BACKGROUND: Acetylation and methylation of histones alter the chromatin structure and accessibility that affect transcriptional regulators binding to enhancers and promoters. The binding of transcriptional regulators enables the interaction between enhancers and promoters, thus affecting gene expression. However, our knowledge of these epigenetic alternations in patients with heart failure remains limited. METHODS AND RESULTS: From the comprehensive analysis of major histone modifications, 3-dimensional chromatin interactions, and transcriptome in left ventricular (LV) tissues from dilated cardiomyopathy (DCM) patients and non-heart failure (NF) donors, differential active enhancer and promoter regions were identified between NF and DCM. Moreover, the genome-wide average promoter signal is significantly lower in DCM than in NF. Super-enhancer (SE) analysis revealed that fewer SEs were found in DCM LVs than in NF ones, and three unique SE-associated genes between NF and DCM were identified. Moreover, SEs are enriched within the genomic region associated with long-range chromatin interactions. The differential enhancer-promoter interactions were observed in the known heart failure gene loci and are correlated with the gene expression levels. Motif analysis identified known cardiac factors and possible novel players for DCM. CONCLUSIONS: We have established the cistrome of four histone modifications and chromatin interactome for enhancers and promoters in NF and DCM tissues. Differential histone modifications and enhancer-promoter interactions were found in DCM, which were associated with gene expression levels of a subset of disease-associated genes in human heart failure.</p>',
			'date' => '2020-06-10',
			'pmid' => 'http://www.pubmed.gov/32533974',
			'doi' => '10.1016/j.yjmcc.2020.06.001',
			'modified' => '2020-08-12 09:30:21',
			'created' => '2020-08-10 12:12:25',
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		),
		(int) 3 => array(
			'id' => '3414',
			'name' => 'SOX4 can redirect TGF-β-mediated SMAD3-transcriptional output in a context-dependent manner to promote tumorigenesis.',
			'authors' => 'Vervoort SJ, Lourenço AR, Tufegdzic Vidakovic A, Mocholi E, Sandoval JL, Rueda OM, Frederiks C, Pals C, Peeters JGC, Caldas C, Bruna A, Coffer PJ',
			'description' => '<p>Expression of the transcription factor SOX4 is often elevated in human cancers, where it generally correlates with tumor-progression and poor-disease outcome. Reduction of SOX4 expression results in both diminished tumor-incidence and metastasis. In breast cancer, TGF-&beta;-mediated induction of SOX4 has been shown to contribute to epithelial-to-mesenchymal transition (EMT), which controls pro-metastatic events. Here, we identify SMAD3 as a novel, functionally relevant SOX4 interaction partner. Genome-wide analysis showed that SOX4 and SMAD3 co-occupy a large number of genomic loci in a cell-type specific manner. Moreover, SOX4 expression was required for TGF-&beta;-mediated induction of a subset of SMAD3/SOX4-co-bound genes regulating migration and extracellular matrix-associated processes, and correlating with poor-prognosis. These findings identify SOX4 as an important SMAD3 co-factor controlling transcription of pro-metastatic genes and context-dependent shaping of the cellular response to TGF-&beta;. Targeted disruption of the interaction between these factors may have the potential to disrupt pro-oncogenic TGF-&beta; signaling, thereby impairing tumorigenesis.</p>',
			'date' => '2018-10-12',
			'pmid' => 'http://www.pubmed.gov/30137431',
			'doi' => '10.1093/nar/gky755',
			'modified' => '2018-12-31 11:20:11',
			'created' => '2018-12-04 09:51:07',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '3397',
			'name' => 'SOX4 inhibits oligodendrocyte differentiation of embryonic neural stem cells in vitro by inducing Hes5 expression',
			'authors' => 'Braccioli Luca, Vervoort Stephin J., Puma Gianmarco, Nijboer Cora H., Coffer Paul J.',
			'description' => '<p>SOX4 has been shown to promote neuronal differentiation both in the adult and embryonic neural progenitors. Ectopic SOX4 expression has also been shown to inhibit oligodendrocyte differentiation in mice, however the underlying molecular mechanisms remain poorly understood. Here we demonstrate that SOX4 regulates transcriptional targets associated with neural development in neural stem cells (NSCs), reducing the expression of genes promoting oligodendrocyte differentiation. Interestingly, we observe that SOX4 levels decreased during oligodendrocyte differentiation in vitro. Moreover, we show that SOX4 knockdown induces increased oligodendrocyte differentiation, as the percentage of Olig2- positive/2',3'-Cyclic-nucleotide 3'-phosphodiesterase (CNPase)-positive maturing oligodendrocytes increases, while the number of Olig2-positive oligodendrocyte precursors is unaffected. Conversely, conditional SOX4 overexpression utilizing a doxycycline inducible system decreases the percentage of maturing oligodendrocytes, suggesting that SOX4 inhibits maturation from precursor to mature oligodendrocyte. We identify the transcription factor Hes5 as a direct SOX4 target gene and we show that conditional overexpression of Hes5 rescues the increased oligodendrocyte differentiation mediated by SOX4 depletion in NSCs. Taken together, these observations support a novel role for SOX4 in NSC by controlling oligodendrocyte differentiation through induction of Hes5 expression.</p>',
			'date' => '2018-10-04',
			'pmid' => 'http://www.pubmed.gov/30343100',
			'doi' => '10.1016/j.scr.2018.10.005',
			'modified' => '2018-11-09 11:52:20',
			'created' => '2018-11-08 12:59:45',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '3424',
			'name' => 'TRPM7 controls mesenchymal features of breast cancer cells by tensional regulation of SOX4.',
			'authors' => 'Kuipers AJ, Middelbeek J, Vrenken K, Pérez-González C, Poelmans G, Klarenbeek J, Jalink K, Trepat X, van Leeuwen FN',
			'description' => '<p>Mechanically induced signaling pathways are important drivers of tumor progression. However, if and how mechanical signals affect metastasis or therapy response remains poorly understood. We previously found that the channel-kinase TRPM7, a regulator of cellular tension implicated in mechano-sensory processes, is required for breast cancer metastasis in vitro and in vivo. Here, we show that TRPM7 contributes to maintaining a mesenchymal phenotype in breast cancer cells by tensional regulation of the EMT transcription factor SOX4. The functional consequences of SOX4 knockdown closely mirror those produced by TRPM7 knockdown. By traction force measurements, we demonstrate that TRPM7 reduces cytoskeletal tension through inhibition of myosin II activity. Moreover, we show that SOX4 expression and downstream mesenchymal markers are inversely regulated by cytoskeletal tension and matrix rigidity. Overall, our results identify SOX4 as a transcription factor that is uniquely sensitive to cellular tension and indicate that TRPM7 may contribute to breast cancer progression by tensional regulation of SOX4.</p>',
			'date' => '2018-07-01',
			'pmid' => 'http://www.pubmed.gov/29684587',
			'doi' => '10.1016/j.bbadis.2018.04.017',
			'modified' => '2018-12-31 11:38:35',
			'created' => '2018-12-04 09:51:07',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '3452',
			'name' => 'Cancer cell specific inhibition of Wnt/β-catenin signaling by forced intracellular acidification.',
			'authors' => 'Melnik S, Dvornikov D, Müller-Decker K, Depner S, Stannek P, Meister M, Warth A, Thomas M, Muley T, Risch A, Plass C, Klingmüller U, Niehrs C, Glinka A',
			'description' => '<p>Use of the diabetes type II drug Metformin is associated with a moderately lowered risk of cancer incidence in numerous tumor entities. Studying the molecular changes associated with the tumor-suppressive action of Metformin we found that the oncogene , which is upregulated in solid tumors and associated with poor prognosis, was induced by Wnt/&beta;-catenin signaling and blocked by Metformin. Wnt signaling inhibition by Metformin was surprisingly specific for cancer cells. Unraveling the underlying specificity, we identified Metformin and other Mitochondrial Complex I (MCI) inhibitors as inducers of intracellular acidification in cancer cells. We demonstrated that acidification triggers the unfolded protein response to induce the global transcriptional repressor , known to block Wnt signaling. Moreover, our results suggest that intracellular acidification universally inhibits Wnt signaling. Based on these findings, we combined MCI inhibitors with H ionophores, to escalate cancer cells into intracellular hyper-acidification and ATP depletion. This treatment lowered intracellular pH both in vitro and in a mouse xenograft tumor model, depleted cellular ATP, blocked Wnt signaling, downregulated , and strongly decreased stemness and viability of cancer cells. Importantly, the inhibition of Wnt signaling occurred downstream of &beta;-catenin, encouraging applications in treatment of cancers caused by and mutations.</p>',
			'date' => '2018-01-01',
			'pmid' => 'http://www.pubmed.gov/29977599',
			'doi' => '10.1038/s41421-018-0033-2',
			'modified' => '2019-02-15 21:43:46',
			'created' => '2019-02-14 15:01:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '2936',
			'name' => 'Sox4 Expression Confers Bladder Cancer Stem Cell Properties and Predicts for Poor Patient Outcome',
			'authors' => 'Shen H et al.',
			'description' => '<p>Genetic and epigenetic alterations have been identified as to contribute directly or indirectly to the generation of transitional cell carcinoma of the urinary bladder (TCC-UB). We have previously found that amplification of chromosome 6p22 is significantly associated with the muscle-invasive rather than superficial TCC-UB. Here, we demonstrated that Sox4, one of the candidate oncogenes located within the chromosome 6p22 amplicon, confers bladder cancer stem cell (CSC) properties. Down-regulation of Sox4 led to the inhibition of cell migration, colony formation as well as mesenchymal-to-epithelial transition (MET). Interestingly, knockdown of Sox4 also reduced the sphere formation, enriched cell population with high levels of aldehyde dehydrogenase (ALDH (high)) and tumor formation potential. Using gene expression profiling, we further identified novel Sox4 target genes. Last, immunohistochemistry analysis of human bladder tumor tissue microarrays (TMAs) indicated that high Sox4 expression was correlated with advanced cancer stages and poor survival rate. In summary, our data show that Sox4 is an important regulator of the bladder CSC properties and it may serve as a biomarker of the aggressive phenotype in bladder cancer.</p>',
			'date' => '2015-11-01',
			'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26681916',
			'doi' => ' 10.7150/ijbs.13240',
			'modified' => '2016-05-26 10:18:21',
			'created' => '2016-05-26 10:18:21',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '687',
			'name' => 'Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.',
			'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
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	'name' => 'Novel transcriptional targets of the SRY-HMG box transcription factor SOX4 link its expression to the development of small cell lung cancer.',
	'authors' => 'Castillo SD, Matheu A, Mariani N, Carretero J, Lopez-Rios F, Lovell-Badge R, Sanchez-Cespedes M',
	'description' => 'The HMG box transcription factor SOX4 involved in neuronal development is amplified and overexpressed in a subset of lung cancers, suggesting that it may be a driver oncogene. In this study, we sought to develop this hypothesis including by defining targets of SOX4 that may mediate its involvement in lung cancer. Ablating SOX4 expression in SOX4-amplified lung cancer cells revealed a gene expression signature that included genes involved in neuronal development such as PCDHB, MYB, RBP1, and TEAD2. Direct recruitment of SOX4 to gene promoters was associated with their upregulation upon ectopic overexpression of SOX4. We confirmed upregulation of the SOX4 expression signature in a panel of primary lung tumors, validating their specific response by a comparison using embryonic fibroblasts from Sox4-deficient mice. Interestingly, we found that small cell lung cancer (SCLC), a subtype of lung cancer with neuroendocrine characteristics, was generally characterized by high levels of SOX2, SOX4, and SOX11 along with the SOX4-specific gene expression signature identified. Taken together, our findings identify a functional role for SOX genes in SCLC, particularly for SOX4 and several novel targets defined in this study.',
	'date' => '2012-01-01',
	'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/22084397',
	'doi' => '',
	'modified' => '2015-07-24 15:38:58',
	'created' => '2015-07-24 15:38:58',
	'ProductsPublication' => array(
		'id' => '4230',
		'product_id' => '3051',
		'publication_id' => '687'
	)
)
$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/22084397" target="_blank"><i class="fa fa-external-link"></i></a>'
include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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