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DiaMag protein A-coated magnetic beads (ChIP-seq grade)

Catalog Number

Format

Price

C03010020-660
(kch-802-660)

660 µl

$250.00

Other format

C03010020-220

220 µl

C03010020-150

1.5 ml

The protein A-coated magnetic beads have been extensively validated in chromatin immunoprecipitation assay (ChIP). These beads are intended for isolation of immune complexes (chromatin and specific antibody) in ChIP experiments performed. The beads are suitable for immunoprecipitation of rabbit polyclonal Abs, mouse IgG2a, IgG2b and IgA, guinea pig IgG, dog IgG, pig IgG. The beads should be washed before use.

特徴
Format
Supplied as a suspension in PBS (pH 7.4), with 0.1% Tween-20 and 0.02% sodium azide.

Storage and stability
Store at 4°C. Do not freeze. Keep the beads in liquid suspension during storage as drying will result in reduced performance.

Precautions
This product is for research use only. Not for use in diagnostic or therapeutic procedures.
資料
Datasheet DiaMag protein A-coated magnetic beads DATASHEET
Datasheet description Download

出版物

How to properly cite this product in your work

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E2F6 initiates stable epigenetic silencing of germline genes duringembryonic development
Dahlet T. et al.
In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to t...

FOS licenses early events in stem cell activation driving skeletal muscleregeneration.
Almada, Albert E. et al.
Muscle satellite cells (SCs) are a quiescent (non-proliferative) stem cell population in uninjured skeletal muscle. Although SCs have been investigated for nearly 60 years, the molecular drivers that transform quiescent SCs into the rapidly dividing (activated) stem/progenitor cells that mediate muscle repair after ...

Inhibition of HIV-1 gene transcription by KAP1 in myeloid lineage.
Ait-Ammar A. et al.
HIV-1 latency generates reservoirs that prevent viral eradication by the current therapies. To find strategies toward an HIV cure, detailed understandings of the molecular mechanisms underlying establishment and persistence of the reservoirs are needed. The cellular transcription factor KAP1 is known as a potent rep...

ZNF354C is a transcriptional repressor that inhibits endothelialangiogenic sprouting.
Oo, James A and Irmer, Barnabas and Günther, Stefan and Warwick, Timothyand Pálfi, Katalin and Izquierdo Ponce, Judit and Teichmann, Tom andPflüger-Müller, Beatrice and Gilsbach, Ralf and Brandes, Ralf P andLeisegang, Matthias S
Zinc finger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specific mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C has so far only been studied in bone and tum...

Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.
Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschen
Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes...

Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma.
Orouji E, Peitsch WK, Orouji A, Houben R, Utikal J
Merkel cell carcinoma (MCC) is a deadly skin cancer, and about 80% of its cases have been shown to harbor integrated Merkel polyomavirus in the tumor cell genome. Viral oncoproteins expressed in the tumor cells are considered as the oncogenic factors of these virus-positive Merkel cell carcinoma (VP-MCC). In contras...

UNBRANCHED3 Expression and Inflorescence Development is Mediated by UNBRANCHED2 and the Distal Enhancer, KRN4, in Maize.
Yanfang Du, Lei Liu, Yong Peng, Manfei Li, Yunfu Li, Dan Liu, Xingwang Li, Zuxin Zhang
Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been...

The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.
Pflüger-Müller B, Oo JA, Heering J, Warwick T, Proschak E, Günther S, Looso M, Rezende F, Fork C, Geisslinger G, Thomas D, Gurke R, Steinhilber D, Schulz M, Leisegang MS, Brandes RP
Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in t...

A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment.
Farhat DC, Swale C, Dard C, Cannella D, Ortet P, Barakat M, Sindikubwabo F, Belmudes L, De Bock PJ, Couté Y, Bougdour A, Hakimi MA
Toxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assi...

Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome.
Cooper A, Butto T, Hammer N, Jagannath S, Fend-Guella DL, Akhtar J, Radyushkin K, Lesage F, Winter J, Strand S, Roeper J, Zechner U, Schweiger S
Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9...

Analysis of Histone Modifications in Rodent Pancreatic Islets by Native Chromatin Immunoprecipitation.
Sandovici I, Nicholas LM, O'Neill LP
The islets of Langerhans are clusters of cells dispersed throughout the pancreas that produce several hormones essential for controlling a variety of metabolic processes, including glucose homeostasis and lipid metabolism. Studying the transcriptional control of pancreatic islet cells has important implications for ...

Unraveling the role of H3K4 trimethylation and lncRNA HOTAIR in SATB1 and DUSP4-dependent survival of virulent Mycobacterium tuberculosis in macrophages
Subuddhi Arijita, Kumar Manish, Majumder Debayan, Sarkar Arijita, Ghosh Zhumur, Vasudevan Madavan, Kundu Manikuntala, Basu Joyoti
The modification of chromatin influences host transcriptional programs during bacterial infection, at times skewing the balance in favor of pathogen survival. To test the role of chromatin modifications during Mycobacterium tuberculosis infection, we analysed genome-wide deposition of H3K4me3 marks in macrophages in...

Epigenetic remodelling licences adult cholangiocytes for organoid formation and liver regeneration.
Aloia L, McKie MA, Vernaz G, Cordero-Espinoza L, Aleksieva N, van den Ameele J, Antonica F, Font-Cunill B, Raven A, Aiese Cigliano R, Belenguer G, Mort RL, Brand AH, Zernicka-Goetz M, Forbes SJ, Miska EA, Huch M
Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring both hepatocytes and cholangiocytes. We recently showed that ductal cells clonally expand as self-renewing liver organoids that retain their differentiation capacity into both hepatocytes and ductal ...

Interleukin-22 protects intestinal stem cells against genotoxic stress.
Gronke K, Hernández PP, Zimmermann J, Klose CSN, Kofoed-Branzk M, Guendel F, Witkowski M, Tizian C, Amann L, Schumacher F, Glatt H, Triantafyllopoulou A, Diefenbach A
Environmental genotoxic factors pose a challenge to the genomic integrity of epithelial cells at barrier surfaces that separate host organisms from the environment. They can induce mutations that, if they occur in epithelial stem cells, contribute to malignant transformation and cancer development. Genome integrity ...

H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum).
Sharma C, Kumar S, Saripalli G, Jain N, Raghuvanshi S, Sharma JB, Prabhu KV, Sharma PK, Balyan HS, Gupta PK
Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the prese...

The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.
Vasconez AE, Janetzko P, Oo JA, Pflüger-Müller B, Ratiu C, Gu L, Helin K, Geisslinger G, Fleming I, Schröder K, Fork C, Brandes RP, Leisegang MS
AIM: The histone demethylase Jarid1b limits gene expression by removing the active methyl mark from histone3 lysine4 at gene promoter regions. A vascular function of Jarid1b is unknown, but a vasoprotective function to inflammatory and hypertrophic stimuli, like angiotensin II (AngII) could be inferred. This hypothe...

Metabolic Induction of Trained Immunity through the Mevalonate Pathway.
Bekkering S, Arts RJW, Novakovic B, Kourtzelis I, van der Heijden CDCC, Li Y, Popa CD, Ter Horst R, van Tuijl J, Netea-Maier RT, van de Veerdonk FL, Chavakis T, Joosten LAB, van der Meer JWM, Stunnenberg H, Riksen NP, Netea MG
Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of...

Genomic Characterization of Metformin Hepatic Response
Luizon M.R. et al.
Metformin is used as a first-line therapy for type 2 diabetes (T2D) and prescribed for numerous other diseases. However, its mechanism of action in the liver has yet to be characterized in a systematic manner. To comprehensively identify genes and regulatory elements associated with metformin treatment, we carried o...

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	'Promotion' => array(),
	'Protocol' => array(),
	'Publication' => array(
		(int) 0 => array(
			'id' => '4318',
			'name' => 'E2F6 initiates stable epigenetic silencing of germline genes duringembryonic development',
			'authors' => 'Dahlet T. et al.',
			'description' => '<p>In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in embryos, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long-term epigenetic silencing during mouse development.</p>',
			'date' => '2021-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34117224',
			'doi' => '10.1038/s41467-021-23596-w',
			'modified' => '2022-08-02 16:53:03',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 1 => array(
			'id' => '4167',
			'name' => 'FOS licenses early events in stem cell activation driving skeletal muscleregeneration.',
			'authors' => 'Almada, Albert E. et al.',
			'description' => '<p>Muscle satellite cells (SCs) are a quiescent (non-proliferative) stem cell population in uninjured skeletal muscle. Although SCs have been investigated for nearly 60 years, the molecular drivers that transform quiescent SCs into the rapidly dividing (activated) stem/progenitor cells that mediate muscle repair after injury remain largely unknown. Here we identify a prominent FBJ osteosarcoma oncogene (Fos) mRNA and protein signature in recently activated SCs that is rapidly, heterogeneously, and transiently induced by muscle damage. We further reveal a requirement for FOS to efficiently initiate key stem cell functions, including cell cycle entry, proliferative expansion, and muscle regeneration, via induction of "pro-regenerative" target genes that stimulate cell migration, division, and differentiation. Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration. This work uncovers an early-activated FOS/ART1/mono-ADP-ribosylation (MARylation) pathway that is essential for stem cell-regenerative responses.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33503437',
			'doi' => '10.1016/j.celrep.2020.108656',
			'modified' => '2021-12-21 15:46:42',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4188',
			'name' => 'Inhibition of HIV-1 gene transcription by KAP1 in myeloid lineage.',
			'authors' => 'Ait-Ammar A. et al.',
			'description' => '<p>HIV-1 latency generates reservoirs that prevent viral eradication by the current therapies. To find strategies toward an HIV cure, detailed understandings of the molecular mechanisms underlying establishment and persistence of the reservoirs are needed. The cellular transcription factor KAP1 is known as a potent repressor of gene transcription. Here we report that KAP1 represses HIV-1 gene expression in myeloid cells including microglial cells, the major reservoir of the central nervous system. Mechanistically, KAP1 interacts and colocalizes with the viral transactivator Tat to promote its degradation via the proteasome pathway and repress HIV-1 gene expression. In myeloid models of latent HIV-1 infection, the depletion of KAP1 increased viral gene elongation and reactivated HIV-1 expression. Bound to the latent HIV-1 promoter, KAP1 associates and cooperates with CTIP2, a key epigenetic silencer of HIV-1 expression in microglial cells. In addition, Tat and CTIP2 compete for KAP1 binding suggesting a dynamic modulation of the KAP1 cellular partners upon HIV-1 infection. Altogether, our results suggest that KAP1 contributes to the establishment and the persistence of HIV-1 latency in myeloid cells.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33514850',
			'doi' => '10.1038/s41598-021-82164-w',
			'modified' => '2022-01-05 15:08:41',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '4095',
			'name' => 'ZNF354C is a transcriptional repressor that inhibits endothelialangiogenic sprouting.',
			'authors' => 'Oo, James A and Irmer, Barnabas and Günther, Stefan and Warwick, Timothyand Pálfi, Katalin and Izquierdo Ponce, Judit and Teichmann, Tom andPflüger-Müller, Beatrice and Gilsbach, Ralf and Brandes, Ralf P andLeisegang, Matthias S',
			'description' => '<p>Zinc finger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specific mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C&nbsp;has so far only been studied in bone and tumour, its function was determined in endothelial cells. ZNF354C is expressed in vascular cells and localises to the nucleus and cytoplasm. Overexpression of ZNF354C in human endothelial cells results in a marked inhibition of endothelial sprouting. RNA-sequencing of human microvascular endothelial cells with and without overexpression of ZNF354C revealed that the protein is a potent transcriptional repressor. ZNF354C contains an active KRAB domain which mediates this suppression as shown by mutagenesis analysis. ZNF354C interacts with dsDNA, TRIM28 and histones, as observed by proximity ligation and immunoprecipitation. Moreover, chromatin immunoprecipitation revealed that the ZNF binds to specific endothelial-relevant target-gene promoters. ZNF354C suppresses these genes as shown by CRISPR/Cas knockout and RNAi. Inhibition of endothelial sprouting by ZNF354C is dependent on the amino acids DV and MLE of the KRAB domain. These results demonstrate that ZNF354C is a repressive transcription factor which acts through a KRAB domain to inhibit endothelial angiogenic sprouting.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33154469',
			'doi' => '10.1038/s41598-020-76193-0',
			'modified' => '2021-03-17 17:19:53',
			'created' => '2021-02-18 10:21:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '3938',
			'name' => 'Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.',
			'authors' => 'Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschen',
			'description' => '<p>Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix&nbsp;forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.</p>',
			'date' => '2020-04-27',
			'pmid' => 'http://www.pubmed.gov/32341350',
			'doi' => '10.1038/s41467-020-15995-2',
			'modified' => '2020-08-17 10:30:19',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '3940',
			'name' => 'Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma.',
			'authors' => 'Orouji E, Peitsch WK, Orouji A, Houben R, Utikal J',
			'description' => '<p>Merkel cell carcinoma (MCC) is a deadly skin cancer, and about 80% of its cases have been shown to harbor integrated Merkel polyomavirus in the tumor cell genome. Viral oncoproteins expressed in the tumor cells are considered as the oncogenic factors of these virus-positive Merkel cell carcinoma (VP-MCC). In contrast, the molecular pathogenesis of virus-negative MCC (VN-MCC) is less well understood. Using gene expression analysis of MCC cell lines, we found histone methyltransferase PRDM8 to be elevated in VN-MCC. This finding was confirmed by immunohistochemical analysis of MCC tumors, revealing that increased PRDM8 expression in VN-MCC is also associated with increased H3K9 methylation. CRISPR-mediated silencing of PRDM8 in MCC cells further supported the histone methylating role of this protein in VN-MCC. We also identified miR-20a-5p as a negative regulator of PRDM8. Taken together, our findings provide insights into the role of PRDM8 as a histone methyltransferase in VN-MCC tumorigenesis.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32344701',
			'doi' => '10.3390/cancers12041057',
			'modified' => '2020-08-17 10:27:34',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '3932',
			'name' => 'UNBRANCHED3 Expression and Inflorescence Development is Mediated by UNBRANCHED2 and the Distal Enhancer, KRN4, in Maize.',
			'authors' => 'Yanfang Du, Lei Liu, Yong Peng, Manfei Li, Yunfu Li, Dan Liu, Xingwang Li, Zuxin Zhang',
			'description' => '<p>Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been characterized genetically. KERNEL ROW NUMBER4 (KRN4), an intergenic quantitative trait locus for kernel row number, is assumed to be a cis-regulatory element of UNBRANCHED3 (UB3), a key inflorescence gene. However, the mechanism by which KRN4 controls UB3 expression remains unclear. Here, we found that KRN4 exhibits an open chromatin state, harboring sequences that showed high enhancer activity toward the 35S and UB3 promoters. KRN4 is bound by UB2-centered transcription complexes and interacts with the UB3 promoter by three duplex interactions to affect UB3 expression. Sequence variation at KRN4 enhances ub2 and ub3 mutant ear fasciation. Therefore, we suggest that KRN4 functions as a distal enhancer of the UB3 promoter via chromatin interactions and recruitment of UB2-centered transcription complexes for the fine-tuning of UB3 expression in meristems of ear inflorescences. These results provide evidence that an intergenic region helps to finely tune gene expression, providing a new perspective on the genetic control of quantitative traits.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32330129',
			'doi' => '10.1371/journal.pgen.1008764',
			'modified' => '2020-08-17 10:40:28',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '3933',
			'name' => 'The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.',
			'authors' => 'Pflüger-Müller B, Oo JA, Heering J, Warwick T, Proschak E, Günther S, Looso M, Rezende F, Fork C, Geisslinger G, Thomas D, Gurke R, Steinhilber D, Schulz M, Leisegang MS, Brandes RP',
			'description' => '<p>Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). In response to combined stimulation with cytokines, IL-1&beta; and TNF&alpha;, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased. AEA pretreatment had profound effects on cytokine-induced gene expression in hVSMC and murine aorta. As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA. This effect was not mediated through AEA-dependent interference of the AP-1 or NF-&kappa;B pathways but rather through an epigenetic mechanism. In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter. These effects were mediated by recruitment of HDAC4 and the nuclear corepressor NCoR1 to the CCL2 promoter. This study therefore establishes a novel anti-inflammatory mechanism for the endogenous endocannabinoid AEA in vascular smooth muscle cells. Furthermore, this work provides a link between endogenous endocannabinoid signaling and epigenetic regulation.</p>',
			'date' => '2020-04-22',
			'pmid' => 'http://www.pubmed.gov/32323032',
			'doi' => '10.1007/s00395-020-0793-3',
			'modified' => '2020-08-17 10:39:12',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '3884',
			'name' => 'A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment.',
			'authors' => 'Farhat DC, Swale C, Dard C, Cannella D, Ortet P, Barakat M, Sindikubwabo F, Belmudes L, De Bock PJ, Couté Y, Bougdour A, Hakimi MA',
			'description' => '<p>Toxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assigned roles for chromatin shapers, including histone modifications, in establishing specific epigenetic programs for each given stage. Here, we identified the T. gondii microrchidia (MORC) protein as an upstream transcriptional repressor of sexual commitment. MORC, in a complex with Apetala 2 (AP2) transcription factors, was shown to recruit the histone deacetylase HDAC3, thereby impeding the accessibility of chromatin at the genes that are exclusively expressed during sexual stages. We found that MORC-depleted cells underwent marked transcriptional changes, resulting in the expression of a specific repertoire of genes, and revealing a shift from asexual proliferation to sexual differentiation. MORC acts as a master regulator that directs the hierarchical expression of secondary AP2 transcription factors, and these transcription factors potentially contribute to the unidirectionality of the life cycle. Thus, MORC plays a cardinal role in the T. gondii life cycle, and its conditional depletion offers a method to study the sexual development of the parasite in vitro, and is proposed as an alternative to the requirement of T. gondii infections in cats.</p>',
			'date' => '2020-02-24',
			'pmid' => 'http://www.pubmed.gov/32094587',
			'doi' => '10.1038/s41564-020-0674-4',
			'modified' => '2020-03-20 17:27:25',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3866',
			'name' => 'Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome.',
			'authors' => 'Cooper A, Butto T, Hammer N, Jagannath S, Fend-Guella DL, Akhtar J, Radyushkin K, Lesage F, Winter J, Strand S, Roeper J, Zechner U, Schweiger S',
			'description' => '<p>Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an imprinting disorder.</p>',
			'date' => '2020-01-24',
			'pmid' => 'http://www.pubmed.gov/31980599',
			'doi' => '10.1038/s41467-019-13918-4',
			'modified' => '2020-03-20 17:50:11',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3802',
			'name' => 'Analysis of Histone Modifications in Rodent Pancreatic Islets by Native Chromatin Immunoprecipitation.',
			'authors' => 'Sandovici I, Nicholas LM, O'Neill LP',
			'description' => '<p>The islets of Langerhans are clusters of cells dispersed throughout the pancreas that produce several hormones essential for controlling a variety of metabolic processes, including glucose homeostasis and lipid metabolism. Studying the transcriptional control of pancreatic islet cells has important implications for understanding the mechanisms that control their normal development, as well as the pathogenesis of metabolic diseases such as diabetes. Histones represent the main protein components of the chromatin and undergo diverse covalent modifications that are very important for gene regulation. Here we describe the isolation of pancreatic islets from rodents and subsequently outline the methods used to immunoprecipitate and analyze the native chromatin obtained from these cells.</p>',
			'date' => '2020-01-01',
			'pmid' => 'http://www.pubmed.gov/31586329',
			'doi' => '10.1007/978-1-4939-9882-1',
			'modified' => '2019-12-05 11:28:01',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3838',
			'name' => 'Unraveling the role of H3K4 trimethylation and lncRNA HOTAIR in SATB1 and DUSP4-dependent survival of virulent Mycobacterium tuberculosis in macrophages',
			'authors' => 'Subuddhi Arijita, Kumar Manish, Majumder Debayan, Sarkar Arijita, Ghosh Zhumur, Vasudevan Madavan, Kundu Manikuntala, Basu Joyoti',
			'description' => '<p>The modification of chromatin influences host transcriptional programs during bacterial infection, at times skewing the balance in favor of pathogen survival. To test the role of chromatin modifications during Mycobacterium tuberculosis infection, we analysed genome-wide deposition of H3K4me3 marks in macrophages infected with either avirulent M. tuberculosis H37Ra or virulent H37Rv, by chromatin immunoprecipitation, followed by sequencing. We validated differences in association of H3K4me3 at the loci of special AT-rich sequence binding protein 1 (SATB1) and dual specificity MAP kinase phosphatase 4 (DUSP4) between H37Rv and H37Ra-infected macrophages, and demonstrated their role in regulating bacterial survival in macrophages as well as the expression of chemokines. SATB1 repressed gp91phox (an NADPH oxidase subunit) thereby regulating reactive oxygen species (ROS) generation during infection. Long non-coding RNA HOX transcript antisense RNA (HOTAIR) was upregulated in H37Ra-, but downregulated in H37Rv-infected macrophages. HOTAIR overexpression correlated with deposition of repressive H3K27me3 marks around the TSSs of DUSP4 and SATB1, suggesting that its downregulation favors the transcription of SATB1 and DUSP4. In summary, we have delineated histone modification- and lncRNA-dependent mechanisms regulating gene expression patterns facilitating survival of virulent M. tuberculosis. Our observations raise the possibility of harnessing histone-modifying enzymes to develop host-directed therapies for tuberculosis.</p>',
			'date' => '2019-12-22',
			'pmid' => 'https://doi.org/10.1016/j.tube.2019.101897',
			'doi' => '10.1016/j.tube.2019.101897',
			'modified' => '2020-02-20 11:22:43',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3807',
			'name' => 'Epigenetic remodelling licences adult cholangiocytes for organoid formation and liver regeneration.',
			'authors' => 'Aloia L, McKie MA, Vernaz G, Cordero-Espinoza L, Aleksieva N, van den Ameele J, Antonica F, Font-Cunill B, Raven A, Aiese Cigliano R, Belenguer G, Mort RL, Brand AH, Zernicka-Goetz M, Forbes SJ, Miska EA, Huch M',
			'description' => '<p>Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring both hepatocytes and cholangiocytes. We recently showed that ductal cells clonally expand as self-renewing liver organoids that retain their differentiation capacity into both hepatocytes and ductal cells. However, the molecular mechanisms by which adult ductal-committed cells acquire cellular plasticity, initiate organoids and regenerate the damaged tissue remain largely unknown. Here, we describe that ductal cells undergo a transient, genome-wide, remodelling of their transcriptome and epigenome during organoid initiation and in vivo following tissue damage. TET1-mediated hydroxymethylation licences differentiated ductal cells to initiate organoids and activate the regenerative programme through the transcriptional regulation of stem-cell genes and regenerative pathways including the YAP-Hippo signalling. Our results argue in favour of the remodelling of genomic methylome/hydroxymethylome landscapes as a general mechanism by which differentiated cells exit a committed state in response to tissue damage.</p>',
			'date' => '2019-11-04',
			'pmid' => 'http://www.pubmed.gov/31685987',
			'doi' => '10.1038/s41556-019-0402-6',
			'modified' => '2019-12-05 11:19:34',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3723',
			'name' => 'Interleukin-22 protects intestinal stem cells against genotoxic stress.',
			'authors' => 'Gronke K, Hernández PP, Zimmermann J, Klose CSN, Kofoed-Branzk M, Guendel F, Witkowski M, Tizian C, Amann L, Schumacher F, Glatt H, Triantafyllopoulou A, Diefenbach A',
			'description' => '<p>Environmental genotoxic factors pose a challenge to the genomic integrity of epithelial cells at barrier surfaces that separate host organisms from the environment. They can induce mutations that, if they occur in epithelial stem cells, contribute to malignant transformation and cancer development. Genome integrity in epithelial stem cells is maintained by an evolutionarily conserved cellular response pathway, the DNA damage response (DDR). The DDR culminates in either transient cell-cycle arrest and DNA repair or elimination of damaged cells by apoptosis. Here we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymphoid cells (ILC3) and &gamma;&delta; T cells, is an important regulator of the DDR machinery in intestinal epithelial stem cells. Using a new mouse model that enables sporadic inactivation of the IL-22 receptor in colon epithelial stem cells, we demonstrate that IL-22 is required for effective initiation of the DDR following DNA damage. Stem cells deprived of IL-22 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained more mutations and were more likely to give rise to colon cancer. We identified metabolites of glucosinolates, a group of phytochemicals contained in cruciferous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells. These metabolites are ligands of the aryl hydrocarbon receptor (AhR), and AhR-mediated signalling in ILC3 and &gamma;&delta; T cells controlled their production of IL-22. Mice fed with diets depleted of glucosinolates produced only very low levels of IL-22 and, consequently, the DDR in epithelial cells of mice on a glucosinolate-free diet was impaired. This work identifies a homeostatic network protecting stem cells against challenge to their genome integrity by AhR-mediated 'sensing' of genotoxic compounds from the diet. AhR signalling, in turn, ensures on-demand production of IL-22 by innate lymphocytes directly regulating components of the DDR in epithelial stem cells.</p>',
			'date' => '2019-02-01',
			'pmid' => 'http://www.pubmed.gov/30700914',
			'doi' => '10.1038/s41586-019-0899-7',
			'modified' => '2019-08-07 10:28:18',
			'created' => '2019-07-31 13:35:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '3500',
			'name' => 'H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum).',
			'authors' => 'Sharma C, Kumar S, Saripalli G, Jain N, Raghuvanshi S, Sharma JB, Prabhu KV, Sharma PK, Balyan HS, Gupta PK',
			'description' => '<p>Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the present study, enrichment of H3K4ac and H3K9ac in promoters of six defense responsive genes (N-acetyltransferase, WRKY 40, WRKY 70, ASR1, Peroxidase 12 and Sarcosine oxidase) was compared with their expression in a pair of near-isogenic lines (NILs) for the gene Lr28 following inoculation with leaf rust pathotype '77-5'; ChIP-qPCR was used for this purpose. The proximal and distal promoters of these genes contained a number of motifs that are known to respond to biotic stresses. The enrichment of two acetylation marks changed with passage of time; changes in expression of two of the six genes (N-acetyltransferase and peroxidase12), largely matched with changes in H3K4/H3K9 acetylation patterns of the two promoter regions. For example, enrichment of both the marks matched with higher expression of N-acetyltransferase gene in susceptible NIL and the deacetylation (H3K4ac) largely matched with reduced gene expression in resistant NIL. In peroxidase12, enrichment of H3K4ac and H3K9ac largely matched with higher expression in both the NILs. In the remaining four genes, changes in H3 acetylation did not always match with gene expression levels. This indicated complexity in the regulation of the expression of these remaining four genes, which may be controlled by other epigenetic/genetic regulatory mechanisms that need further analysis.</p>',
			'date' => '2018-10-08',
			'pmid' => 'http://www.pubmed.org/30298213',
			'doi' => '10.1007/s00438-018-1500-z',
			'modified' => '2019-02-27 16:25:07',
			'created' => '2019-02-27 12:54:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3407',
			'name' => 'The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.',
			'authors' => 'Vasconez AE, Janetzko P, Oo JA, Pflüger-Müller B, Ratiu C, Gu L, Helin K, Geisslinger G, Fleming I, Schröder K, Fork C, Brandes RP, Leisegang MS',
			'description' => '<p>AIM: The histone demethylase Jarid1b limits gene expression by removing the active methyl mark from histone3 lysine4 at gene promoter regions. A vascular function of Jarid1b is unknown, but a vasoprotective function to inflammatory and hypertrophic stimuli, like angiotensin II (AngII) could be inferred. This hypothesis was tested using Jarid1b knockout mice and the inhibitor PBIT. METHODS: Mice or aortic segments were treated with AngII to induce endothelial dysfunction. Aortae from WT and Jarid1b knockout were studied in organ chambers and endothelium-dependent dilator responses to acetylcholine and endothelium-independent responses to DetaNONOate were recorded after pre-constriction with phenylephrine in the presence or absence of the NO-synthase inhibitor nitro-L-arginine. Molecular mechanisms were investigated with chromatin immunoprecipitation, RNA-Seq, RNA-3'-adaptor-ligation, actinomycin D and RNA-immunoprecipitation. RESULTS: Knockout or inhibition of Jarid1b prevented the development of endothelial dysfunction in response to AngII. This effect was not a consequence of altered nitrite oxide availability but accompanied by a loss of the inflammatory response to AngII. As Jarid1b mainly inhibits gene expression, an indirect effect should account for this observation. AngII induced the soluble epoxide hydrolase (sEH), which degrades anti-inflammatory lipids, and thus promotes inflammation. Knockout or inhibition of Jarid1b prevented the AngII-mediated sEH induction. Mechanistically, Jarid1b maintained the length of the 3'untranslated region of the sEH mRNA, thereby increasing its stability and thus sEH protein expression. Loss of Jarid1b activity therefore resulted in sEH mRNA destabilization. CONCLUSION: Jarid1b contributes to the pro-inflammatory effects of AngII by stabilizing sEH expression. Jarid1b inhibition might be an option for future therapeutics against cardiovascular dysfunction.</p>',
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			'description' => '<p>Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of cholesterol itself, is essential for training of myeloid cells. Rather, the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways. Statins, which block mevalonate generation, prevent trained immunity induction. Furthermore, monocytes of patients with hyper immunoglobulin D syndrome (HIDS), who are mevalonate kinase deficient and accumulate mevalonate, have a constitutive trained immunity phenotype at both immunological and epigenetic levels, which could explain the attacks of sterile inflammation that these patients experience. Unraveling the role of mevalonate in trained immunity contributes to our understanding of the pathophysiology of HIDS and identifies novel therapeutic targets for clinical conditions with excessive activation of trained immunity.</p>',
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$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/27902686" 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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			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34117224',
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			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33503437',
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			'description' => '<p>HIV-1 latency generates reservoirs that prevent viral eradication by the current therapies. To find strategies toward an HIV cure, detailed understandings of the molecular mechanisms underlying establishment and persistence of the reservoirs are needed. The cellular transcription factor KAP1 is known as a potent repressor of gene transcription. Here we report that KAP1 represses HIV-1 gene expression in myeloid cells including microglial cells, the major reservoir of the central nervous system. Mechanistically, KAP1 interacts and colocalizes with the viral transactivator Tat to promote its degradation via the proteasome pathway and repress HIV-1 gene expression. In myeloid models of latent HIV-1 infection, the depletion of KAP1 increased viral gene elongation and reactivated HIV-1 expression. Bound to the latent HIV-1 promoter, KAP1 associates and cooperates with CTIP2, a key epigenetic silencer of HIV-1 expression in microglial cells. In addition, Tat and CTIP2 compete for KAP1 binding suggesting a dynamic modulation of the KAP1 cellular partners upon HIV-1 infection. Altogether, our results suggest that KAP1 contributes to the establishment and the persistence of HIV-1 latency in myeloid cells.</p>',
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			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33514850',
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			'authors' => 'Oo, James A and Irmer, Barnabas and Günther, Stefan and Warwick, Timothyand Pálfi, Katalin and Izquierdo Ponce, Judit and Teichmann, Tom andPflüger-Müller, Beatrice and Gilsbach, Ralf and Brandes, Ralf P andLeisegang, Matthias S',
			'description' => '<p>Zinc finger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specific mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C&nbsp;has so far only been studied in bone and tumour, its function was determined in endothelial cells. ZNF354C is expressed in vascular cells and localises to the nucleus and cytoplasm. Overexpression of ZNF354C in human endothelial cells results in a marked inhibition of endothelial sprouting. RNA-sequencing of human microvascular endothelial cells with and without overexpression of ZNF354C revealed that the protein is a potent transcriptional repressor. ZNF354C contains an active KRAB domain which mediates this suppression as shown by mutagenesis analysis. ZNF354C interacts with dsDNA, TRIM28 and histones, as observed by proximity ligation and immunoprecipitation. Moreover, chromatin immunoprecipitation revealed that the ZNF binds to specific endothelial-relevant target-gene promoters. ZNF354C suppresses these genes as shown by CRISPR/Cas knockout and RNAi. Inhibition of endothelial sprouting by ZNF354C is dependent on the amino acids DV and MLE of the KRAB domain. These results demonstrate that ZNF354C is a repressive transcription factor which acts through a KRAB domain to inhibit endothelial angiogenic sprouting.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33154469',
			'doi' => '10.1038/s41598-020-76193-0',
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			'name' => 'Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.',
			'authors' => 'Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschen',
			'description' => '<p>Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix&nbsp;forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.</p>',
			'date' => '2020-04-27',
			'pmid' => 'http://www.pubmed.gov/32341350',
			'doi' => '10.1038/s41467-020-15995-2',
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			'id' => '3940',
			'name' => 'Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma.',
			'authors' => 'Orouji E, Peitsch WK, Orouji A, Houben R, Utikal J',
			'description' => '<p>Merkel cell carcinoma (MCC) is a deadly skin cancer, and about 80% of its cases have been shown to harbor integrated Merkel polyomavirus in the tumor cell genome. Viral oncoproteins expressed in the tumor cells are considered as the oncogenic factors of these virus-positive Merkel cell carcinoma (VP-MCC). In contrast, the molecular pathogenesis of virus-negative MCC (VN-MCC) is less well understood. Using gene expression analysis of MCC cell lines, we found histone methyltransferase PRDM8 to be elevated in VN-MCC. This finding was confirmed by immunohistochemical analysis of MCC tumors, revealing that increased PRDM8 expression in VN-MCC is also associated with increased H3K9 methylation. CRISPR-mediated silencing of PRDM8 in MCC cells further supported the histone methylating role of this protein in VN-MCC. We also identified miR-20a-5p as a negative regulator of PRDM8. Taken together, our findings provide insights into the role of PRDM8 as a histone methyltransferase in VN-MCC tumorigenesis.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32344701',
			'doi' => '10.3390/cancers12041057',
			'modified' => '2020-08-17 10:27:34',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '3932',
			'name' => 'UNBRANCHED3 Expression and Inflorescence Development is Mediated by UNBRANCHED2 and the Distal Enhancer, KRN4, in Maize.',
			'authors' => 'Yanfang Du, Lei Liu, Yong Peng, Manfei Li, Yunfu Li, Dan Liu, Xingwang Li, Zuxin Zhang',
			'description' => '<p>Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been characterized genetically. KERNEL ROW NUMBER4 (KRN4), an intergenic quantitative trait locus for kernel row number, is assumed to be a cis-regulatory element of UNBRANCHED3 (UB3), a key inflorescence gene. However, the mechanism by which KRN4 controls UB3 expression remains unclear. Here, we found that KRN4 exhibits an open chromatin state, harboring sequences that showed high enhancer activity toward the 35S and UB3 promoters. KRN4 is bound by UB2-centered transcription complexes and interacts with the UB3 promoter by three duplex interactions to affect UB3 expression. Sequence variation at KRN4 enhances ub2 and ub3 mutant ear fasciation. Therefore, we suggest that KRN4 functions as a distal enhancer of the UB3 promoter via chromatin interactions and recruitment of UB2-centered transcription complexes for the fine-tuning of UB3 expression in meristems of ear inflorescences. These results provide evidence that an intergenic region helps to finely tune gene expression, providing a new perspective on the genetic control of quantitative traits.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32330129',
			'doi' => '10.1371/journal.pgen.1008764',
			'modified' => '2020-08-17 10:40:28',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '3933',
			'name' => 'The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.',
			'authors' => 'Pflüger-Müller B, Oo JA, Heering J, Warwick T, Proschak E, Günther S, Looso M, Rezende F, Fork C, Geisslinger G, Thomas D, Gurke R, Steinhilber D, Schulz M, Leisegang MS, Brandes RP',
			'description' => '<p>Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). In response to combined stimulation with cytokines, IL-1&beta; and TNF&alpha;, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased. AEA pretreatment had profound effects on cytokine-induced gene expression in hVSMC and murine aorta. As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA. This effect was not mediated through AEA-dependent interference of the AP-1 or NF-&kappa;B pathways but rather through an epigenetic mechanism. In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter. These effects were mediated by recruitment of HDAC4 and the nuclear corepressor NCoR1 to the CCL2 promoter. This study therefore establishes a novel anti-inflammatory mechanism for the endogenous endocannabinoid AEA in vascular smooth muscle cells. Furthermore, this work provides a link between endogenous endocannabinoid signaling and epigenetic regulation.</p>',
			'date' => '2020-04-22',
			'pmid' => 'http://www.pubmed.gov/32323032',
			'doi' => '10.1007/s00395-020-0793-3',
			'modified' => '2020-08-17 10:39:12',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '3884',
			'name' => 'A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment.',
			'authors' => 'Farhat DC, Swale C, Dard C, Cannella D, Ortet P, Barakat M, Sindikubwabo F, Belmudes L, De Bock PJ, Couté Y, Bougdour A, Hakimi MA',
			'description' => '<p>Toxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assigned roles for chromatin shapers, including histone modifications, in establishing specific epigenetic programs for each given stage. Here, we identified the T. gondii microrchidia (MORC) protein as an upstream transcriptional repressor of sexual commitment. MORC, in a complex with Apetala 2 (AP2) transcription factors, was shown to recruit the histone deacetylase HDAC3, thereby impeding the accessibility of chromatin at the genes that are exclusively expressed during sexual stages. We found that MORC-depleted cells underwent marked transcriptional changes, resulting in the expression of a specific repertoire of genes, and revealing a shift from asexual proliferation to sexual differentiation. MORC acts as a master regulator that directs the hierarchical expression of secondary AP2 transcription factors, and these transcription factors potentially contribute to the unidirectionality of the life cycle. Thus, MORC plays a cardinal role in the T. gondii life cycle, and its conditional depletion offers a method to study the sexual development of the parasite in vitro, and is proposed as an alternative to the requirement of T. gondii infections in cats.</p>',
			'date' => '2020-02-24',
			'pmid' => 'http://www.pubmed.gov/32094587',
			'doi' => '10.1038/s41564-020-0674-4',
			'modified' => '2020-03-20 17:27:25',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3866',
			'name' => 'Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome.',
			'authors' => 'Cooper A, Butto T, Hammer N, Jagannath S, Fend-Guella DL, Akhtar J, Radyushkin K, Lesage F, Winter J, Strand S, Roeper J, Zechner U, Schweiger S',
			'description' => '<p>Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an imprinting disorder.</p>',
			'date' => '2020-01-24',
			'pmid' => 'http://www.pubmed.gov/31980599',
			'doi' => '10.1038/s41467-019-13918-4',
			'modified' => '2020-03-20 17:50:11',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3802',
			'name' => 'Analysis of Histone Modifications in Rodent Pancreatic Islets by Native Chromatin Immunoprecipitation.',
			'authors' => 'Sandovici I, Nicholas LM, O'Neill LP',
			'description' => '<p>The islets of Langerhans are clusters of cells dispersed throughout the pancreas that produce several hormones essential for controlling a variety of metabolic processes, including glucose homeostasis and lipid metabolism. Studying the transcriptional control of pancreatic islet cells has important implications for understanding the mechanisms that control their normal development, as well as the pathogenesis of metabolic diseases such as diabetes. Histones represent the main protein components of the chromatin and undergo diverse covalent modifications that are very important for gene regulation. Here we describe the isolation of pancreatic islets from rodents and subsequently outline the methods used to immunoprecipitate and analyze the native chromatin obtained from these cells.</p>',
			'date' => '2020-01-01',
			'pmid' => 'http://www.pubmed.gov/31586329',
			'doi' => '10.1007/978-1-4939-9882-1',
			'modified' => '2019-12-05 11:28:01',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3838',
			'name' => 'Unraveling the role of H3K4 trimethylation and lncRNA HOTAIR in SATB1 and DUSP4-dependent survival of virulent Mycobacterium tuberculosis in macrophages',
			'authors' => 'Subuddhi Arijita, Kumar Manish, Majumder Debayan, Sarkar Arijita, Ghosh Zhumur, Vasudevan Madavan, Kundu Manikuntala, Basu Joyoti',
			'description' => '<p>The modification of chromatin influences host transcriptional programs during bacterial infection, at times skewing the balance in favor of pathogen survival. To test the role of chromatin modifications during Mycobacterium tuberculosis infection, we analysed genome-wide deposition of H3K4me3 marks in macrophages infected with either avirulent M. tuberculosis H37Ra or virulent H37Rv, by chromatin immunoprecipitation, followed by sequencing. We validated differences in association of H3K4me3 at the loci of special AT-rich sequence binding protein 1 (SATB1) and dual specificity MAP kinase phosphatase 4 (DUSP4) between H37Rv and H37Ra-infected macrophages, and demonstrated their role in regulating bacterial survival in macrophages as well as the expression of chemokines. SATB1 repressed gp91phox (an NADPH oxidase subunit) thereby regulating reactive oxygen species (ROS) generation during infection. Long non-coding RNA HOX transcript antisense RNA (HOTAIR) was upregulated in H37Ra-, but downregulated in H37Rv-infected macrophages. HOTAIR overexpression correlated with deposition of repressive H3K27me3 marks around the TSSs of DUSP4 and SATB1, suggesting that its downregulation favors the transcription of SATB1 and DUSP4. In summary, we have delineated histone modification- and lncRNA-dependent mechanisms regulating gene expression patterns facilitating survival of virulent M. tuberculosis. Our observations raise the possibility of harnessing histone-modifying enzymes to develop host-directed therapies for tuberculosis.</p>',
			'date' => '2019-12-22',
			'pmid' => 'https://doi.org/10.1016/j.tube.2019.101897',
			'doi' => '10.1016/j.tube.2019.101897',
			'modified' => '2020-02-20 11:22:43',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3807',
			'name' => 'Epigenetic remodelling licences adult cholangiocytes for organoid formation and liver regeneration.',
			'authors' => 'Aloia L, McKie MA, Vernaz G, Cordero-Espinoza L, Aleksieva N, van den Ameele J, Antonica F, Font-Cunill B, Raven A, Aiese Cigliano R, Belenguer G, Mort RL, Brand AH, Zernicka-Goetz M, Forbes SJ, Miska EA, Huch M',
			'description' => '<p>Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring both hepatocytes and cholangiocytes. We recently showed that ductal cells clonally expand as self-renewing liver organoids that retain their differentiation capacity into both hepatocytes and ductal cells. However, the molecular mechanisms by which adult ductal-committed cells acquire cellular plasticity, initiate organoids and regenerate the damaged tissue remain largely unknown. Here, we describe that ductal cells undergo a transient, genome-wide, remodelling of their transcriptome and epigenome during organoid initiation and in vivo following tissue damage. TET1-mediated hydroxymethylation licences differentiated ductal cells to initiate organoids and activate the regenerative programme through the transcriptional regulation of stem-cell genes and regenerative pathways including the YAP-Hippo signalling. Our results argue in favour of the remodelling of genomic methylome/hydroxymethylome landscapes as a general mechanism by which differentiated cells exit a committed state in response to tissue damage.</p>',
			'date' => '2019-11-04',
			'pmid' => 'http://www.pubmed.gov/31685987',
			'doi' => '10.1038/s41556-019-0402-6',
			'modified' => '2019-12-05 11:19:34',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3723',
			'name' => 'Interleukin-22 protects intestinal stem cells against genotoxic stress.',
			'authors' => 'Gronke K, Hernández PP, Zimmermann J, Klose CSN, Kofoed-Branzk M, Guendel F, Witkowski M, Tizian C, Amann L, Schumacher F, Glatt H, Triantafyllopoulou A, Diefenbach A',
			'description' => '<p>Environmental genotoxic factors pose a challenge to the genomic integrity of epithelial cells at barrier surfaces that separate host organisms from the environment. They can induce mutations that, if they occur in epithelial stem cells, contribute to malignant transformation and cancer development. Genome integrity in epithelial stem cells is maintained by an evolutionarily conserved cellular response pathway, the DNA damage response (DDR). The DDR culminates in either transient cell-cycle arrest and DNA repair or elimination of damaged cells by apoptosis. Here we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymphoid cells (ILC3) and &gamma;&delta; T cells, is an important regulator of the DDR machinery in intestinal epithelial stem cells. Using a new mouse model that enables sporadic inactivation of the IL-22 receptor in colon epithelial stem cells, we demonstrate that IL-22 is required for effective initiation of the DDR following DNA damage. Stem cells deprived of IL-22 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained more mutations and were more likely to give rise to colon cancer. We identified metabolites of glucosinolates, a group of phytochemicals contained in cruciferous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells. These metabolites are ligands of the aryl hydrocarbon receptor (AhR), and AhR-mediated signalling in ILC3 and &gamma;&delta; T cells controlled their production of IL-22. Mice fed with diets depleted of glucosinolates produced only very low levels of IL-22 and, consequently, the DDR in epithelial cells of mice on a glucosinolate-free diet was impaired. This work identifies a homeostatic network protecting stem cells against challenge to their genome integrity by AhR-mediated 'sensing' of genotoxic compounds from the diet. AhR signalling, in turn, ensures on-demand production of IL-22 by innate lymphocytes directly regulating components of the DDR in epithelial stem cells.</p>',
			'date' => '2019-02-01',
			'pmid' => 'http://www.pubmed.gov/30700914',
			'doi' => '10.1038/s41586-019-0899-7',
			'modified' => '2019-08-07 10:28:18',
			'created' => '2019-07-31 13:35:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '3500',
			'name' => 'H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum).',
			'authors' => 'Sharma C, Kumar S, Saripalli G, Jain N, Raghuvanshi S, Sharma JB, Prabhu KV, Sharma PK, Balyan HS, Gupta PK',
			'description' => '<p>Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the present study, enrichment of H3K4ac and H3K9ac in promoters of six defense responsive genes (N-acetyltransferase, WRKY 40, WRKY 70, ASR1, Peroxidase 12 and Sarcosine oxidase) was compared with their expression in a pair of near-isogenic lines (NILs) for the gene Lr28 following inoculation with leaf rust pathotype '77-5'; ChIP-qPCR was used for this purpose. The proximal and distal promoters of these genes contained a number of motifs that are known to respond to biotic stresses. The enrichment of two acetylation marks changed with passage of time; changes in expression of two of the six genes (N-acetyltransferase and peroxidase12), largely matched with changes in H3K4/H3K9 acetylation patterns of the two promoter regions. For example, enrichment of both the marks matched with higher expression of N-acetyltransferase gene in susceptible NIL and the deacetylation (H3K4ac) largely matched with reduced gene expression in resistant NIL. In peroxidase12, enrichment of H3K4ac and H3K9ac largely matched with higher expression in both the NILs. In the remaining four genes, changes in H3 acetylation did not always match with gene expression levels. This indicated complexity in the regulation of the expression of these remaining four genes, which may be controlled by other epigenetic/genetic regulatory mechanisms that need further analysis.</p>',
			'date' => '2018-10-08',
			'pmid' => 'http://www.pubmed.org/30298213',
			'doi' => '10.1007/s00438-018-1500-z',
			'modified' => '2019-02-27 16:25:07',
			'created' => '2019-02-27 12:54:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3407',
			'name' => 'The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.',
			'authors' => 'Vasconez AE, Janetzko P, Oo JA, Pflüger-Müller B, Ratiu C, Gu L, Helin K, Geisslinger G, Fleming I, Schröder K, Fork C, Brandes RP, Leisegang MS',
			'description' => '<p>AIM: The histone demethylase Jarid1b limits gene expression by removing the active methyl mark from histone3 lysine4 at gene promoter regions. A vascular function of Jarid1b is unknown, but a vasoprotective function to inflammatory and hypertrophic stimuli, like angiotensin II (AngII) could be inferred. This hypothesis was tested using Jarid1b knockout mice and the inhibitor PBIT. METHODS: Mice or aortic segments were treated with AngII to induce endothelial dysfunction. Aortae from WT and Jarid1b knockout were studied in organ chambers and endothelium-dependent dilator responses to acetylcholine and endothelium-independent responses to DetaNONOate were recorded after pre-constriction with phenylephrine in the presence or absence of the NO-synthase inhibitor nitro-L-arginine. Molecular mechanisms were investigated with chromatin immunoprecipitation, RNA-Seq, RNA-3'-adaptor-ligation, actinomycin D and RNA-immunoprecipitation. RESULTS: Knockout or inhibition of Jarid1b prevented the development of endothelial dysfunction in response to AngII. This effect was not a consequence of altered nitrite oxide availability but accompanied by a loss of the inflammatory response to AngII. As Jarid1b mainly inhibits gene expression, an indirect effect should account for this observation. AngII induced the soluble epoxide hydrolase (sEH), which degrades anti-inflammatory lipids, and thus promotes inflammation. Knockout or inhibition of Jarid1b prevented the AngII-mediated sEH induction. Mechanistically, Jarid1b maintained the length of the 3'untranslated region of the sEH mRNA, thereby increasing its stability and thus sEH protein expression. Loss of Jarid1b activity therefore resulted in sEH mRNA destabilization. CONCLUSION: Jarid1b contributes to the pro-inflammatory effects of AngII by stabilizing sEH expression. Jarid1b inhibition might be an option for future therapeutics against cardiovascular dysfunction.</p>',
			'date' => '2018-08-04',
			'pmid' => 'http://www.pubmed.gov/30076673',
			'doi' => '10.1111/apha.13168',
			'modified' => '2018-11-09 11:18:29',
			'created' => '2018-11-08 12:59:45',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '3446',
			'name' => 'Metabolic Induction of Trained Immunity through the Mevalonate Pathway.',
			'authors' => 'Bekkering S, Arts RJW, Novakovic B, Kourtzelis I, van der Heijden CDCC, Li Y, Popa CD, Ter Horst R, van Tuijl J, Netea-Maier RT, van de Veerdonk FL, Chavakis T, Joosten LAB, van der Meer JWM, Stunnenberg H, Riksen NP, Netea MG',
			'description' => '<p>Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of cholesterol itself, is essential for training of myeloid cells. Rather, the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways. Statins, which block mevalonate generation, prevent trained immunity induction. Furthermore, monocytes of patients with hyper immunoglobulin D syndrome (HIDS), who are mevalonate kinase deficient and accumulate mevalonate, have a constitutive trained immunity phenotype at both immunological and epigenetic levels, which could explain the attacks of sterile inflammation that these patients experience. Unraveling the role of mevalonate in trained immunity contributes to our understanding of the pathophysiology of HIDS and identifies novel therapeutic targets for clinical conditions with excessive activation of trained immunity.</p>',
			'date' => '2018-01-11',
			'pmid' => 'http://www.pubmed.gov/29328908',
			'doi' => '10.1016/j.cell.2017.11.025',
			'modified' => '2019-02-15 21:37:39',
			'created' => '2019-02-14 15:01:22',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '3085',
			'name' => 'Genomic Characterization of Metformin Hepatic Response',
			'authors' => 'Luizon M.R. et al.',
			'description' => '<p>Metformin is used as a first-line therapy for type 2 diabetes (T2D) and prescribed for numerous other diseases. However, its mechanism of action in the liver has yet to be characterized in a systematic manner. To comprehensively identify genes and regulatory elements associated with metformin treatment, we carried out RNA-seq and ChIP-seq (H3K27ac, H3K27me3) on primary human hepatocytes from the same donor treated with vehicle control, metformin or metformin and compound C, an AMP-activated protein kinase (AMPK) inhibitor (allowing to identify AMPK-independent pathways). We identified thousands of metformin responsive AMPK-dependent and AMPK-independent differentially expressed genes and regulatory elements. We functionally validated several elements for metformin-induced promoter and enhancer activity. These include an enhancer in an ataxia telangiectasia mutated (ATM) intron that has SNPs in linkage disequilibrium with a metformin treatment response GWAS lead SNP (rs11212617) that showed increased enhancer activity for the associated haplotype. Expression quantitative trait locus (eQTL) liver analysis and CRISPR activation suggest that this enhancer could be regulating ATM, which has a known role in AMPK activation, and potentially also EXPH5 and DDX10, its neighboring genes. Using ChIP-seq and siRNA knockdown, we further show that activating transcription factor 3 (ATF3), our top metformin upregulated AMPK-dependent gene, could have an important role in gluconeogenesis repression. Our findings provide a genome-wide representation of metformin hepatic response, highlight important sequences that could be associated with interindividual variability in glycemic response to metformin and identify novel T2D treatment candidates.</p>',
			'date' => '2016-11-30',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27902686',
			'doi' => '',
			'modified' => '2016-12-20 10:41:29',
			'created' => '2016-12-20 10:41:29',
			'ProductsPublication' => array(
				[maximum depth reached]
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<p><strong>Precautions</strong><br /> This product is for research use only. Not for use in diagnostic or therapeutic procedures.</p>
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<p><strong>Storage and stability</strong><br /> Store at 4&deg;C. Do not freeze. Keep the beads in liquid suspension during storage as drying will result in reduced performance.</p>
<p><strong>Precautions</strong><br /> This product is for research use only. Not for use in diagnostic or therapeutic procedures.</p>',
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			'id' => '4318',
			'name' => 'E2F6 initiates stable epigenetic silencing of germline genes duringembryonic development',
			'authors' => 'Dahlet T. et al.',
			'description' => '<p>In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in embryos, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long-term epigenetic silencing during mouse development.</p>',
			'date' => '2021-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34117224',
			'doi' => '10.1038/s41467-021-23596-w',
			'modified' => '2022-08-02 16:53:03',
			'created' => '2022-05-19 10:41:50',
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			'name' => 'FOS licenses early events in stem cell activation driving skeletal muscleregeneration.',
			'authors' => 'Almada, Albert E. et al.',
			'description' => '<p>Muscle satellite cells (SCs) are a quiescent (non-proliferative) stem cell population in uninjured skeletal muscle. Although SCs have been investigated for nearly 60 years, the molecular drivers that transform quiescent SCs into the rapidly dividing (activated) stem/progenitor cells that mediate muscle repair after injury remain largely unknown. Here we identify a prominent FBJ osteosarcoma oncogene (Fos) mRNA and protein signature in recently activated SCs that is rapidly, heterogeneously, and transiently induced by muscle damage. We further reveal a requirement for FOS to efficiently initiate key stem cell functions, including cell cycle entry, proliferative expansion, and muscle regeneration, via induction of "pro-regenerative" target genes that stimulate cell migration, division, and differentiation. Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration. This work uncovers an early-activated FOS/ART1/mono-ADP-ribosylation (MARylation) pathway that is essential for stem cell-regenerative responses.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33503437',
			'doi' => '10.1016/j.celrep.2020.108656',
			'modified' => '2021-12-21 15:46:42',
			'created' => '2021-12-06 15:53:19',
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			'id' => '4188',
			'name' => 'Inhibition of HIV-1 gene transcription by KAP1 in myeloid lineage.',
			'authors' => 'Ait-Ammar A. et al.',
			'description' => '<p>HIV-1 latency generates reservoirs that prevent viral eradication by the current therapies. To find strategies toward an HIV cure, detailed understandings of the molecular mechanisms underlying establishment and persistence of the reservoirs are needed. The cellular transcription factor KAP1 is known as a potent repressor of gene transcription. Here we report that KAP1 represses HIV-1 gene expression in myeloid cells including microglial cells, the major reservoir of the central nervous system. Mechanistically, KAP1 interacts and colocalizes with the viral transactivator Tat to promote its degradation via the proteasome pathway and repress HIV-1 gene expression. In myeloid models of latent HIV-1 infection, the depletion of KAP1 increased viral gene elongation and reactivated HIV-1 expression. Bound to the latent HIV-1 promoter, KAP1 associates and cooperates with CTIP2, a key epigenetic silencer of HIV-1 expression in microglial cells. In addition, Tat and CTIP2 compete for KAP1 binding suggesting a dynamic modulation of the KAP1 cellular partners upon HIV-1 infection. Altogether, our results suggest that KAP1 contributes to the establishment and the persistence of HIV-1 latency in myeloid cells.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33514850',
			'doi' => '10.1038/s41598-021-82164-w',
			'modified' => '2022-01-05 15:08:41',
			'created' => '2021-12-06 15:53:19',
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		(int) 3 => array(
			'id' => '4095',
			'name' => 'ZNF354C is a transcriptional repressor that inhibits endothelialangiogenic sprouting.',
			'authors' => 'Oo, James A and Irmer, Barnabas and Günther, Stefan and Warwick, Timothyand Pálfi, Katalin and Izquierdo Ponce, Judit and Teichmann, Tom andPflüger-Müller, Beatrice and Gilsbach, Ralf and Brandes, Ralf P andLeisegang, Matthias S',
			'description' => '<p>Zinc finger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specific mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C&nbsp;has so far only been studied in bone and tumour, its function was determined in endothelial cells. ZNF354C is expressed in vascular cells and localises to the nucleus and cytoplasm. Overexpression of ZNF354C in human endothelial cells results in a marked inhibition of endothelial sprouting. RNA-sequencing of human microvascular endothelial cells with and without overexpression of ZNF354C revealed that the protein is a potent transcriptional repressor. ZNF354C contains an active KRAB domain which mediates this suppression as shown by mutagenesis analysis. ZNF354C interacts with dsDNA, TRIM28 and histones, as observed by proximity ligation and immunoprecipitation. Moreover, chromatin immunoprecipitation revealed that the ZNF binds to specific endothelial-relevant target-gene promoters. ZNF354C suppresses these genes as shown by CRISPR/Cas knockout and RNAi. Inhibition of endothelial sprouting by ZNF354C is dependent on the amino acids DV and MLE of the KRAB domain. These results demonstrate that ZNF354C is a repressive transcription factor which acts through a KRAB domain to inhibit endothelial angiogenic sprouting.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33154469',
			'doi' => '10.1038/s41598-020-76193-0',
			'modified' => '2021-03-17 17:19:53',
			'created' => '2021-02-18 10:21:53',
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		),
		(int) 4 => array(
			'id' => '3938',
			'name' => 'Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.',
			'authors' => 'Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschen',
			'description' => '<p>Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix&nbsp;forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.</p>',
			'date' => '2020-04-27',
			'pmid' => 'http://www.pubmed.gov/32341350',
			'doi' => '10.1038/s41467-020-15995-2',
			'modified' => '2020-08-17 10:30:19',
			'created' => '2020-08-10 12:12:25',
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		(int) 5 => array(
			'id' => '3940',
			'name' => 'Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma.',
			'authors' => 'Orouji E, Peitsch WK, Orouji A, Houben R, Utikal J',
			'description' => '<p>Merkel cell carcinoma (MCC) is a deadly skin cancer, and about 80% of its cases have been shown to harbor integrated Merkel polyomavirus in the tumor cell genome. Viral oncoproteins expressed in the tumor cells are considered as the oncogenic factors of these virus-positive Merkel cell carcinoma (VP-MCC). In contrast, the molecular pathogenesis of virus-negative MCC (VN-MCC) is less well understood. Using gene expression analysis of MCC cell lines, we found histone methyltransferase PRDM8 to be elevated in VN-MCC. This finding was confirmed by immunohistochemical analysis of MCC tumors, revealing that increased PRDM8 expression in VN-MCC is also associated with increased H3K9 methylation. CRISPR-mediated silencing of PRDM8 in MCC cells further supported the histone methylating role of this protein in VN-MCC. We also identified miR-20a-5p as a negative regulator of PRDM8. Taken together, our findings provide insights into the role of PRDM8 as a histone methyltransferase in VN-MCC tumorigenesis.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32344701',
			'doi' => '10.3390/cancers12041057',
			'modified' => '2020-08-17 10:27:34',
			'created' => '2020-08-10 12:12:25',
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		),
		(int) 6 => array(
			'id' => '3932',
			'name' => 'UNBRANCHED3 Expression and Inflorescence Development is Mediated by UNBRANCHED2 and the Distal Enhancer, KRN4, in Maize.',
			'authors' => 'Yanfang Du, Lei Liu, Yong Peng, Manfei Li, Yunfu Li, Dan Liu, Xingwang Li, Zuxin Zhang',
			'description' => '<p>Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been characterized genetically. KERNEL ROW NUMBER4 (KRN4), an intergenic quantitative trait locus for kernel row number, is assumed to be a cis-regulatory element of UNBRANCHED3 (UB3), a key inflorescence gene. However, the mechanism by which KRN4 controls UB3 expression remains unclear. Here, we found that KRN4 exhibits an open chromatin state, harboring sequences that showed high enhancer activity toward the 35S and UB3 promoters. KRN4 is bound by UB2-centered transcription complexes and interacts with the UB3 promoter by three duplex interactions to affect UB3 expression. Sequence variation at KRN4 enhances ub2 and ub3 mutant ear fasciation. Therefore, we suggest that KRN4 functions as a distal enhancer of the UB3 promoter via chromatin interactions and recruitment of UB2-centered transcription complexes for the fine-tuning of UB3 expression in meristems of ear inflorescences. These results provide evidence that an intergenic region helps to finely tune gene expression, providing a new perspective on the genetic control of quantitative traits.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32330129',
			'doi' => '10.1371/journal.pgen.1008764',
			'modified' => '2020-08-17 10:40:28',
			'created' => '2020-08-10 12:12:25',
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		(int) 7 => array(
			'id' => '3933',
			'name' => 'The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.',
			'authors' => 'Pflüger-Müller B, Oo JA, Heering J, Warwick T, Proschak E, Günther S, Looso M, Rezende F, Fork C, Geisslinger G, Thomas D, Gurke R, Steinhilber D, Schulz M, Leisegang MS, Brandes RP',
			'description' => '<p>Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). In response to combined stimulation with cytokines, IL-1&beta; and TNF&alpha;, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased. AEA pretreatment had profound effects on cytokine-induced gene expression in hVSMC and murine aorta. As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA. This effect was not mediated through AEA-dependent interference of the AP-1 or NF-&kappa;B pathways but rather through an epigenetic mechanism. In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter. These effects were mediated by recruitment of HDAC4 and the nuclear corepressor NCoR1 to the CCL2 promoter. This study therefore establishes a novel anti-inflammatory mechanism for the endogenous endocannabinoid AEA in vascular smooth muscle cells. Furthermore, this work provides a link between endogenous endocannabinoid signaling and epigenetic regulation.</p>',
			'date' => '2020-04-22',
			'pmid' => 'http://www.pubmed.gov/32323032',
			'doi' => '10.1007/s00395-020-0793-3',
			'modified' => '2020-08-17 10:39:12',
			'created' => '2020-08-10 12:12:25',
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		),
		(int) 8 => array(
			'id' => '3884',
			'name' => 'A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment.',
			'authors' => 'Farhat DC, Swale C, Dard C, Cannella D, Ortet P, Barakat M, Sindikubwabo F, Belmudes L, De Bock PJ, Couté Y, Bougdour A, Hakimi MA',
			'description' => '<p>Toxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assigned roles for chromatin shapers, including histone modifications, in establishing specific epigenetic programs for each given stage. Here, we identified the T. gondii microrchidia (MORC) protein as an upstream transcriptional repressor of sexual commitment. MORC, in a complex with Apetala 2 (AP2) transcription factors, was shown to recruit the histone deacetylase HDAC3, thereby impeding the accessibility of chromatin at the genes that are exclusively expressed during sexual stages. We found that MORC-depleted cells underwent marked transcriptional changes, resulting in the expression of a specific repertoire of genes, and revealing a shift from asexual proliferation to sexual differentiation. MORC acts as a master regulator that directs the hierarchical expression of secondary AP2 transcription factors, and these transcription factors potentially contribute to the unidirectionality of the life cycle. Thus, MORC plays a cardinal role in the T. gondii life cycle, and its conditional depletion offers a method to study the sexual development of the parasite in vitro, and is proposed as an alternative to the requirement of T. gondii infections in cats.</p>',
			'date' => '2020-02-24',
			'pmid' => 'http://www.pubmed.gov/32094587',
			'doi' => '10.1038/s41564-020-0674-4',
			'modified' => '2020-03-20 17:27:25',
			'created' => '2020-03-13 13:45:54',
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		(int) 9 => array(
			'id' => '3866',
			'name' => 'Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome.',
			'authors' => 'Cooper A, Butto T, Hammer N, Jagannath S, Fend-Guella DL, Akhtar J, Radyushkin K, Lesage F, Winter J, Strand S, Roeper J, Zechner U, Schweiger S',
			'description' => '<p>Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an imprinting disorder.</p>',
			'date' => '2020-01-24',
			'pmid' => 'http://www.pubmed.gov/31980599',
			'doi' => '10.1038/s41467-019-13918-4',
			'modified' => '2020-03-20 17:50:11',
			'created' => '2020-03-13 13:45:54',
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		),
		(int) 10 => array(
			'id' => '3802',
			'name' => 'Analysis of Histone Modifications in Rodent Pancreatic Islets by Native Chromatin Immunoprecipitation.',
			'authors' => 'Sandovici I, Nicholas LM, O'Neill LP',
			'description' => '<p>The islets of Langerhans are clusters of cells dispersed throughout the pancreas that produce several hormones essential for controlling a variety of metabolic processes, including glucose homeostasis and lipid metabolism. Studying the transcriptional control of pancreatic islet cells has important implications for understanding the mechanisms that control their normal development, as well as the pathogenesis of metabolic diseases such as diabetes. Histones represent the main protein components of the chromatin and undergo diverse covalent modifications that are very important for gene regulation. Here we describe the isolation of pancreatic islets from rodents and subsequently outline the methods used to immunoprecipitate and analyze the native chromatin obtained from these cells.</p>',
			'date' => '2020-01-01',
			'pmid' => 'http://www.pubmed.gov/31586329',
			'doi' => '10.1007/978-1-4939-9882-1',
			'modified' => '2019-12-05 11:28:01',
			'created' => '2019-12-02 15:25:44',
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		(int) 11 => array(
			'id' => '3838',
			'name' => 'Unraveling the role of H3K4 trimethylation and lncRNA HOTAIR in SATB1 and DUSP4-dependent survival of virulent Mycobacterium tuberculosis in macrophages',
			'authors' => 'Subuddhi Arijita, Kumar Manish, Majumder Debayan, Sarkar Arijita, Ghosh Zhumur, Vasudevan Madavan, Kundu Manikuntala, Basu Joyoti',
			'description' => '<p>The modification of chromatin influences host transcriptional programs during bacterial infection, at times skewing the balance in favor of pathogen survival. To test the role of chromatin modifications during Mycobacterium tuberculosis infection, we analysed genome-wide deposition of H3K4me3 marks in macrophages infected with either avirulent M. tuberculosis H37Ra or virulent H37Rv, by chromatin immunoprecipitation, followed by sequencing. We validated differences in association of H3K4me3 at the loci of special AT-rich sequence binding protein 1 (SATB1) and dual specificity MAP kinase phosphatase 4 (DUSP4) between H37Rv and H37Ra-infected macrophages, and demonstrated their role in regulating bacterial survival in macrophages as well as the expression of chemokines. SATB1 repressed gp91phox (an NADPH oxidase subunit) thereby regulating reactive oxygen species (ROS) generation during infection. Long non-coding RNA HOX transcript antisense RNA (HOTAIR) was upregulated in H37Ra-, but downregulated in H37Rv-infected macrophages. HOTAIR overexpression correlated with deposition of repressive H3K27me3 marks around the TSSs of DUSP4 and SATB1, suggesting that its downregulation favors the transcription of SATB1 and DUSP4. In summary, we have delineated histone modification- and lncRNA-dependent mechanisms regulating gene expression patterns facilitating survival of virulent M. tuberculosis. Our observations raise the possibility of harnessing histone-modifying enzymes to develop host-directed therapies for tuberculosis.</p>',
			'date' => '2019-12-22',
			'pmid' => 'https://doi.org/10.1016/j.tube.2019.101897',
			'doi' => '10.1016/j.tube.2019.101897',
			'modified' => '2020-02-20 11:22:43',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
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		),
		(int) 12 => array(
			'id' => '3807',
			'name' => 'Epigenetic remodelling licences adult cholangiocytes for organoid formation and liver regeneration.',
			'authors' => 'Aloia L, McKie MA, Vernaz G, Cordero-Espinoza L, Aleksieva N, van den Ameele J, Antonica F, Font-Cunill B, Raven A, Aiese Cigliano R, Belenguer G, Mort RL, Brand AH, Zernicka-Goetz M, Forbes SJ, Miska EA, Huch M',
			'description' => '<p>Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring both hepatocytes and cholangiocytes. We recently showed that ductal cells clonally expand as self-renewing liver organoids that retain their differentiation capacity into both hepatocytes and ductal cells. However, the molecular mechanisms by which adult ductal-committed cells acquire cellular plasticity, initiate organoids and regenerate the damaged tissue remain largely unknown. Here, we describe that ductal cells undergo a transient, genome-wide, remodelling of their transcriptome and epigenome during organoid initiation and in vivo following tissue damage. TET1-mediated hydroxymethylation licences differentiated ductal cells to initiate organoids and activate the regenerative programme through the transcriptional regulation of stem-cell genes and regenerative pathways including the YAP-Hippo signalling. Our results argue in favour of the remodelling of genomic methylome/hydroxymethylome landscapes as a general mechanism by which differentiated cells exit a committed state in response to tissue damage.</p>',
			'date' => '2019-11-04',
			'pmid' => 'http://www.pubmed.gov/31685987',
			'doi' => '10.1038/s41556-019-0402-6',
			'modified' => '2019-12-05 11:19:34',
			'created' => '2019-12-02 15:25:44',
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			'id' => '3723',
			'name' => 'Interleukin-22 protects intestinal stem cells against genotoxic stress.',
			'authors' => 'Gronke K, Hernández PP, Zimmermann J, Klose CSN, Kofoed-Branzk M, Guendel F, Witkowski M, Tizian C, Amann L, Schumacher F, Glatt H, Triantafyllopoulou A, Diefenbach A',
			'description' => '<p>Environmental genotoxic factors pose a challenge to the genomic integrity of epithelial cells at barrier surfaces that separate host organisms from the environment. They can induce mutations that, if they occur in epithelial stem cells, contribute to malignant transformation and cancer development. Genome integrity in epithelial stem cells is maintained by an evolutionarily conserved cellular response pathway, the DNA damage response (DDR). The DDR culminates in either transient cell-cycle arrest and DNA repair or elimination of damaged cells by apoptosis. Here we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymphoid cells (ILC3) and &gamma;&delta; T cells, is an important regulator of the DDR machinery in intestinal epithelial stem cells. Using a new mouse model that enables sporadic inactivation of the IL-22 receptor in colon epithelial stem cells, we demonstrate that IL-22 is required for effective initiation of the DDR following DNA damage. Stem cells deprived of IL-22 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained more mutations and were more likely to give rise to colon cancer. We identified metabolites of glucosinolates, a group of phytochemicals contained in cruciferous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells. These metabolites are ligands of the aryl hydrocarbon receptor (AhR), and AhR-mediated signalling in ILC3 and &gamma;&delta; T cells controlled their production of IL-22. Mice fed with diets depleted of glucosinolates produced only very low levels of IL-22 and, consequently, the DDR in epithelial cells of mice on a glucosinolate-free diet was impaired. This work identifies a homeostatic network protecting stem cells against challenge to their genome integrity by AhR-mediated 'sensing' of genotoxic compounds from the diet. AhR signalling, in turn, ensures on-demand production of IL-22 by innate lymphocytes directly regulating components of the DDR in epithelial stem cells.</p>',
			'date' => '2019-02-01',
			'pmid' => 'http://www.pubmed.gov/30700914',
			'doi' => '10.1038/s41586-019-0899-7',
			'modified' => '2019-08-07 10:28:18',
			'created' => '2019-07-31 13:35:50',
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		(int) 14 => array(
			'id' => '3500',
			'name' => 'H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum).',
			'authors' => 'Sharma C, Kumar S, Saripalli G, Jain N, Raghuvanshi S, Sharma JB, Prabhu KV, Sharma PK, Balyan HS, Gupta PK',
			'description' => '<p>Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the present study, enrichment of H3K4ac and H3K9ac in promoters of six defense responsive genes (N-acetyltransferase, WRKY 40, WRKY 70, ASR1, Peroxidase 12 and Sarcosine oxidase) was compared with their expression in a pair of near-isogenic lines (NILs) for the gene Lr28 following inoculation with leaf rust pathotype '77-5'; ChIP-qPCR was used for this purpose. The proximal and distal promoters of these genes contained a number of motifs that are known to respond to biotic stresses. The enrichment of two acetylation marks changed with passage of time; changes in expression of two of the six genes (N-acetyltransferase and peroxidase12), largely matched with changes in H3K4/H3K9 acetylation patterns of the two promoter regions. For example, enrichment of both the marks matched with higher expression of N-acetyltransferase gene in susceptible NIL and the deacetylation (H3K4ac) largely matched with reduced gene expression in resistant NIL. In peroxidase12, enrichment of H3K4ac and H3K9ac largely matched with higher expression in both the NILs. In the remaining four genes, changes in H3 acetylation did not always match with gene expression levels. This indicated complexity in the regulation of the expression of these remaining four genes, which may be controlled by other epigenetic/genetic regulatory mechanisms that need further analysis.</p>',
			'date' => '2018-10-08',
			'pmid' => 'http://www.pubmed.org/30298213',
			'doi' => '10.1007/s00438-018-1500-z',
			'modified' => '2019-02-27 16:25:07',
			'created' => '2019-02-27 12:54:44',
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			'id' => '3407',
			'name' => 'The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.',
			'authors' => 'Vasconez AE, Janetzko P, Oo JA, Pflüger-Müller B, Ratiu C, Gu L, Helin K, Geisslinger G, Fleming I, Schröder K, Fork C, Brandes RP, Leisegang MS',
			'description' => '<p>AIM: The histone demethylase Jarid1b limits gene expression by removing the active methyl mark from histone3 lysine4 at gene promoter regions. A vascular function of Jarid1b is unknown, but a vasoprotective function to inflammatory and hypertrophic stimuli, like angiotensin II (AngII) could be inferred. This hypothesis was tested using Jarid1b knockout mice and the inhibitor PBIT. METHODS: Mice or aortic segments were treated with AngII to induce endothelial dysfunction. Aortae from WT and Jarid1b knockout were studied in organ chambers and endothelium-dependent dilator responses to acetylcholine and endothelium-independent responses to DetaNONOate were recorded after pre-constriction with phenylephrine in the presence or absence of the NO-synthase inhibitor nitro-L-arginine. Molecular mechanisms were investigated with chromatin immunoprecipitation, RNA-Seq, RNA-3'-adaptor-ligation, actinomycin D and RNA-immunoprecipitation. RESULTS: Knockout or inhibition of Jarid1b prevented the development of endothelial dysfunction in response to AngII. This effect was not a consequence of altered nitrite oxide availability but accompanied by a loss of the inflammatory response to AngII. As Jarid1b mainly inhibits gene expression, an indirect effect should account for this observation. AngII induced the soluble epoxide hydrolase (sEH), which degrades anti-inflammatory lipids, and thus promotes inflammation. Knockout or inhibition of Jarid1b prevented the AngII-mediated sEH induction. Mechanistically, Jarid1b maintained the length of the 3'untranslated region of the sEH mRNA, thereby increasing its stability and thus sEH protein expression. Loss of Jarid1b activity therefore resulted in sEH mRNA destabilization. CONCLUSION: Jarid1b contributes to the pro-inflammatory effects of AngII by stabilizing sEH expression. Jarid1b inhibition might be an option for future therapeutics against cardiovascular dysfunction.</p>',
			'date' => '2018-08-04',
			'pmid' => 'http://www.pubmed.gov/30076673',
			'doi' => '10.1111/apha.13168',
			'modified' => '2018-11-09 11:18:29',
			'created' => '2018-11-08 12:59:45',
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		(int) 16 => array(
			'id' => '3446',
			'name' => 'Metabolic Induction of Trained Immunity through the Mevalonate Pathway.',
			'authors' => 'Bekkering S, Arts RJW, Novakovic B, Kourtzelis I, van der Heijden CDCC, Li Y, Popa CD, Ter Horst R, van Tuijl J, Netea-Maier RT, van de Veerdonk FL, Chavakis T, Joosten LAB, van der Meer JWM, Stunnenberg H, Riksen NP, Netea MG',
			'description' => '<p>Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of cholesterol itself, is essential for training of myeloid cells. Rather, the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways. Statins, which block mevalonate generation, prevent trained immunity induction. Furthermore, monocytes of patients with hyper immunoglobulin D syndrome (HIDS), who are mevalonate kinase deficient and accumulate mevalonate, have a constitutive trained immunity phenotype at both immunological and epigenetic levels, which could explain the attacks of sterile inflammation that these patients experience. Unraveling the role of mevalonate in trained immunity contributes to our understanding of the pathophysiology of HIDS and identifies novel therapeutic targets for clinical conditions with excessive activation of trained immunity.</p>',
			'date' => '2018-01-11',
			'pmid' => 'http://www.pubmed.gov/29328908',
			'doi' => '10.1016/j.cell.2017.11.025',
			'modified' => '2019-02-15 21:37:39',
			'created' => '2019-02-14 15:01:22',
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			'id' => '3085',
			'name' => 'Genomic Characterization of Metformin Hepatic Response',
			'authors' => 'Luizon M.R. et al.',
			'description' => '<p>Metformin is used as a first-line therapy for type 2 diabetes (T2D) and prescribed for numerous other diseases. However, its mechanism of action in the liver has yet to be characterized in a systematic manner. To comprehensively identify genes and regulatory elements associated with metformin treatment, we carried out RNA-seq and ChIP-seq (H3K27ac, H3K27me3) on primary human hepatocytes from the same donor treated with vehicle control, metformin or metformin and compound C, an AMP-activated protein kinase (AMPK) inhibitor (allowing to identify AMPK-independent pathways). We identified thousands of metformin responsive AMPK-dependent and AMPK-independent differentially expressed genes and regulatory elements. We functionally validated several elements for metformin-induced promoter and enhancer activity. These include an enhancer in an ataxia telangiectasia mutated (ATM) intron that has SNPs in linkage disequilibrium with a metformin treatment response GWAS lead SNP (rs11212617) that showed increased enhancer activity for the associated haplotype. Expression quantitative trait locus (eQTL) liver analysis and CRISPR activation suggest that this enhancer could be regulating ATM, which has a known role in AMPK activation, and potentially also EXPH5 and DDX10, its neighboring genes. Using ChIP-seq and siRNA knockdown, we further show that activating transcription factor 3 (ATF3), our top metformin upregulated AMPK-dependent gene, could have an important role in gluconeogenesis repression. Our findings provide a genome-wide representation of metformin hepatic response, highlight important sequences that could be associated with interindividual variability in glycemic response to metformin and identify novel T2D treatment candidates.</p>',
			'date' => '2016-11-30',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27902686',
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<p><strong>Storage and stability</strong><br /> Store at 4&deg;C. Do not freeze. Keep the beads in liquid suspension during storage as drying will result in reduced performance.</p>
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<p><strong>Precautions</strong><br /> This product is for research use only. Not for use in diagnostic or therapeutic procedures.</p>',
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View::_evaluate() - CORE/Cake/View/View.php, line 971
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View::render() - CORE/Cake/View/View.php, line 473
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ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
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			'url' => 'files/products/reagents/Datasheet_DiaMag_protein_A-coated_magnetic_beads.pdf',
			'slug' => 'datasheet-diamag-protein-a-coated-magnetic-beads',
			'meta_keywords' => null,
			'meta_description' => null,
			'modified' => '2015-07-07 11:47:43',
			'created' => '2015-07-07 11:47:43',
			'ProductsDocument' => array(
				[maximum depth reached]
			)
		)
	),
	'Feature' => array(),
	'Image' => array(),
	'Promotion' => array(),
	'Protocol' => array(),
	'Publication' => array(
		(int) 0 => array(
			'id' => '4318',
			'name' => 'E2F6 initiates stable epigenetic silencing of germline genes duringembryonic development',
			'authors' => 'Dahlet T. et al.',
			'description' => '<p>In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in embryos, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long-term epigenetic silencing during mouse development.</p>',
			'date' => '2021-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34117224',
			'doi' => '10.1038/s41467-021-23596-w',
			'modified' => '2022-08-02 16:53:03',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 1 => array(
			'id' => '4167',
			'name' => 'FOS licenses early events in stem cell activation driving skeletal muscleregeneration.',
			'authors' => 'Almada, Albert E. et al.',
			'description' => '<p>Muscle satellite cells (SCs) are a quiescent (non-proliferative) stem cell population in uninjured skeletal muscle. Although SCs have been investigated for nearly 60 years, the molecular drivers that transform quiescent SCs into the rapidly dividing (activated) stem/progenitor cells that mediate muscle repair after injury remain largely unknown. Here we identify a prominent FBJ osteosarcoma oncogene (Fos) mRNA and protein signature in recently activated SCs that is rapidly, heterogeneously, and transiently induced by muscle damage. We further reveal a requirement for FOS to efficiently initiate key stem cell functions, including cell cycle entry, proliferative expansion, and muscle regeneration, via induction of "pro-regenerative" target genes that stimulate cell migration, division, and differentiation. Disruption of one of these Fos/AP-1 targets, NAD(+)-consuming mono-ADP-ribosyl-transferase 1 (Art1), in SCs delays cell cycle entry and impedes progenitor cell expansion and muscle regeneration. This work uncovers an early-activated FOS/ART1/mono-ADP-ribosylation (MARylation) pathway that is essential for stem cell-regenerative responses.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33503437',
			'doi' => '10.1016/j.celrep.2020.108656',
			'modified' => '2021-12-21 15:46:42',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4188',
			'name' => 'Inhibition of HIV-1 gene transcription by KAP1 in myeloid lineage.',
			'authors' => 'Ait-Ammar A. et al.',
			'description' => '<p>HIV-1 latency generates reservoirs that prevent viral eradication by the current therapies. To find strategies toward an HIV cure, detailed understandings of the molecular mechanisms underlying establishment and persistence of the reservoirs are needed. The cellular transcription factor KAP1 is known as a potent repressor of gene transcription. Here we report that KAP1 represses HIV-1 gene expression in myeloid cells including microglial cells, the major reservoir of the central nervous system. Mechanistically, KAP1 interacts and colocalizes with the viral transactivator Tat to promote its degradation via the proteasome pathway and repress HIV-1 gene expression. In myeloid models of latent HIV-1 infection, the depletion of KAP1 increased viral gene elongation and reactivated HIV-1 expression. Bound to the latent HIV-1 promoter, KAP1 associates and cooperates with CTIP2, a key epigenetic silencer of HIV-1 expression in microglial cells. In addition, Tat and CTIP2 compete for KAP1 binding suggesting a dynamic modulation of the KAP1 cellular partners upon HIV-1 infection. Altogether, our results suggest that KAP1 contributes to the establishment and the persistence of HIV-1 latency in myeloid cells.</p>',
			'date' => '2021-01-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33514850',
			'doi' => '10.1038/s41598-021-82164-w',
			'modified' => '2022-01-05 15:08:41',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '4095',
			'name' => 'ZNF354C is a transcriptional repressor that inhibits endothelialangiogenic sprouting.',
			'authors' => 'Oo, James A and Irmer, Barnabas and Günther, Stefan and Warwick, Timothyand Pálfi, Katalin and Izquierdo Ponce, Judit and Teichmann, Tom andPflüger-Müller, Beatrice and Gilsbach, Ralf and Brandes, Ralf P andLeisegang, Matthias S',
			'description' => '<p>Zinc finger proteins (ZNF) are a large group of transcription factors with diverse functions. We recently discovered that endothelial cells harbour a specific mechanism to limit the action of ZNF354C, whose function in endothelial cells is unknown. Given that ZNF354C&nbsp;has so far only been studied in bone and tumour, its function was determined in endothelial cells. ZNF354C is expressed in vascular cells and localises to the nucleus and cytoplasm. Overexpression of ZNF354C in human endothelial cells results in a marked inhibition of endothelial sprouting. RNA-sequencing of human microvascular endothelial cells with and without overexpression of ZNF354C revealed that the protein is a potent transcriptional repressor. ZNF354C contains an active KRAB domain which mediates this suppression as shown by mutagenesis analysis. ZNF354C interacts with dsDNA, TRIM28 and histones, as observed by proximity ligation and immunoprecipitation. Moreover, chromatin immunoprecipitation revealed that the ZNF binds to specific endothelial-relevant target-gene promoters. ZNF354C suppresses these genes as shown by CRISPR/Cas knockout and RNAi. Inhibition of endothelial sprouting by ZNF354C is dependent on the amino acids DV and MLE of the KRAB domain. These results demonstrate that ZNF354C is a repressive transcription factor which acts through a KRAB domain to inhibit endothelial angiogenic sprouting.</p>',
			'date' => '2020-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33154469',
			'doi' => '10.1038/s41598-020-76193-0',
			'modified' => '2021-03-17 17:19:53',
			'created' => '2021-02-18 10:21:53',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '3938',
			'name' => 'Aging-regulated anti-apoptotic long non-coding RNA Sarrah augments recovery from acute myocardial infarction.',
			'authors' => 'Trembinski DJ, Bink DI, Theodorou K, Sommer J, Fischer A, van Bergen A, Kuo CC, Costa IG, Schürmann C, Leisegang MS, Brandes RP, Alekseeva T, Brill B, Wietelmann A, Johnson CN, Spring-Connell A, Kaulich M, Werfel S, Engelhardt S, Hirt MN, Yorgan K, Eschen',
			'description' => '<p>Long non-coding RNAs (lncRNAs) contribute to cardiac (patho)physiology. Aging is the major risk factor for cardiovascular disease with cardiomyocyte apoptosis as one underlying cause. Here, we report the identification of the aging-regulated lncRNA Sarrah (ENSMUST00000140003) that is anti-apoptotic in cardiomyocytes. Importantly, loss of SARRAH (OXCT1-AS1) in human engineered heart tissue results in impaired contractile force development. SARRAH directly binds to the promoters of genes downregulated after SARRAH silencing via RNA-DNA triple helix formation and cardiomyocytes lacking the triple helix&nbsp;forming domain of Sarrah show an increase in apoptosis. One of the direct SARRAH targets is NRF2, and restoration of NRF2 levels after SARRAH silencing partially rescues the reduction in cell viability. Overexpression of Sarrah in mice shows better recovery of cardiac contractile function after AMI compared to control mice. In summary, we identified the anti-apoptotic evolutionary conserved lncRNA Sarrah, which is downregulated by aging, as a regulator of cardiomyocyte survival.</p>',
			'date' => '2020-04-27',
			'pmid' => 'http://www.pubmed.gov/32341350',
			'doi' => '10.1038/s41467-020-15995-2',
			'modified' => '2020-08-17 10:30:19',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '3940',
			'name' => 'Unique Role of Histone Methyltransferase PRDM8 in the Tumorigenesis of Virus-Negative Merkel Cell Carcinoma.',
			'authors' => 'Orouji E, Peitsch WK, Orouji A, Houben R, Utikal J',
			'description' => '<p>Merkel cell carcinoma (MCC) is a deadly skin cancer, and about 80% of its cases have been shown to harbor integrated Merkel polyomavirus in the tumor cell genome. Viral oncoproteins expressed in the tumor cells are considered as the oncogenic factors of these virus-positive Merkel cell carcinoma (VP-MCC). In contrast, the molecular pathogenesis of virus-negative MCC (VN-MCC) is less well understood. Using gene expression analysis of MCC cell lines, we found histone methyltransferase PRDM8 to be elevated in VN-MCC. This finding was confirmed by immunohistochemical analysis of MCC tumors, revealing that increased PRDM8 expression in VN-MCC is also associated with increased H3K9 methylation. CRISPR-mediated silencing of PRDM8 in MCC cells further supported the histone methylating role of this protein in VN-MCC. We also identified miR-20a-5p as a negative regulator of PRDM8. Taken together, our findings provide insights into the role of PRDM8 as a histone methyltransferase in VN-MCC tumorigenesis.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32344701',
			'doi' => '10.3390/cancers12041057',
			'modified' => '2020-08-17 10:27:34',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '3932',
			'name' => 'UNBRANCHED3 Expression and Inflorescence Development is Mediated by UNBRANCHED2 and the Distal Enhancer, KRN4, in Maize.',
			'authors' => 'Yanfang Du, Lei Liu, Yong Peng, Manfei Li, Yunfu Li, Dan Liu, Xingwang Li, Zuxin Zhang',
			'description' => '<p>Enhancers are cis-acting DNA segments with the ability to increase target gene expression. They show high sensitivity to DNase and contain specific DNA elements in an open chromatin state that allows the binding of transcription factors (TFs). While numerous enhancers are annotated in the maize genome, few have been characterized genetically. KERNEL ROW NUMBER4 (KRN4), an intergenic quantitative trait locus for kernel row number, is assumed to be a cis-regulatory element of UNBRANCHED3 (UB3), a key inflorescence gene. However, the mechanism by which KRN4 controls UB3 expression remains unclear. Here, we found that KRN4 exhibits an open chromatin state, harboring sequences that showed high enhancer activity toward the 35S and UB3 promoters. KRN4 is bound by UB2-centered transcription complexes and interacts with the UB3 promoter by three duplex interactions to affect UB3 expression. Sequence variation at KRN4 enhances ub2 and ub3 mutant ear fasciation. Therefore, we suggest that KRN4 functions as a distal enhancer of the UB3 promoter via chromatin interactions and recruitment of UB2-centered transcription complexes for the fine-tuning of UB3 expression in meristems of ear inflorescences. These results provide evidence that an intergenic region helps to finely tune gene expression, providing a new perspective on the genetic control of quantitative traits.</p>',
			'date' => '2020-04-24',
			'pmid' => 'http://www.pubmed.gov/32330129',
			'doi' => '10.1371/journal.pgen.1008764',
			'modified' => '2020-08-17 10:40:28',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '3933',
			'name' => 'The endocannabinoid anandamide has an anti-inflammatory effect on CCL2 expression in vascular smooth muscle cells.',
			'authors' => 'Pflüger-Müller B, Oo JA, Heering J, Warwick T, Proschak E, Günther S, Looso M, Rezende F, Fork C, Geisslinger G, Thomas D, Gurke R, Steinhilber D, Schulz M, Leisegang MS, Brandes RP',
			'description' => '<p>Endocannabinoids are important lipid-signaling mediators. Both protective and deleterious effects of endocannabinoids in the cardiovascular system have been reported but the mechanistic basis for these contradicting observations is unclear. We set out to identify anti-inflammatory mechanisms of endocannabinoids in the murine aorta and in human vascular smooth muscle cells (hVSMC). In response to combined stimulation with cytokines, IL-1&beta; and TNF&alpha;, the murine aorta released several endocannabinoids, with anandamide (AEA) levels being the most significantly increased. AEA pretreatment had profound effects on cytokine-induced gene expression in hVSMC and murine aorta. As revealed by RNA-Seq analysis, the induction of a subset of 21 inflammatory target genes, including the important cytokine CCL2 was blocked by AEA. This effect was not mediated through AEA-dependent interference of the AP-1 or NF-&kappa;B pathways but rather through an epigenetic mechanism. In the presence of AEA, ATAC-Seq analysis and chromatin-immunoprecipitations revealed that CCL2 induction was blocked due to increased levels of H3K27me3 and a decrease of H3K27ac leading to compacted chromatin structure in the CCL2 promoter. These effects were mediated by recruitment of HDAC4 and the nuclear corepressor NCoR1 to the CCL2 promoter. This study therefore establishes a novel anti-inflammatory mechanism for the endogenous endocannabinoid AEA in vascular smooth muscle cells. Furthermore, this work provides a link between endogenous endocannabinoid signaling and epigenetic regulation.</p>',
			'date' => '2020-04-22',
			'pmid' => 'http://www.pubmed.gov/32323032',
			'doi' => '10.1007/s00395-020-0793-3',
			'modified' => '2020-08-17 10:39:12',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '3884',
			'name' => 'A MORC-driven transcriptional switch controls Toxoplasma developmental trajectories and sexual commitment.',
			'authors' => 'Farhat DC, Swale C, Dard C, Cannella D, Ortet P, Barakat M, Sindikubwabo F, Belmudes L, De Bock PJ, Couté Y, Bougdour A, Hakimi MA',
			'description' => '<p>Toxoplasma gondii has a complex life cycle that is typified by asexual development that takes place in vertebrates, and sexual reproduction, which occurs exclusively in felids and is therefore less studied. The developmental transitions rely on changes in the patterns of gene expression, and recent studies have assigned roles for chromatin shapers, including histone modifications, in establishing specific epigenetic programs for each given stage. Here, we identified the T. gondii microrchidia (MORC) protein as an upstream transcriptional repressor of sexual commitment. MORC, in a complex with Apetala 2 (AP2) transcription factors, was shown to recruit the histone deacetylase HDAC3, thereby impeding the accessibility of chromatin at the genes that are exclusively expressed during sexual stages. We found that MORC-depleted cells underwent marked transcriptional changes, resulting in the expression of a specific repertoire of genes, and revealing a shift from asexual proliferation to sexual differentiation. MORC acts as a master regulator that directs the hierarchical expression of secondary AP2 transcription factors, and these transcription factors potentially contribute to the unidirectionality of the life cycle. Thus, MORC plays a cardinal role in the T. gondii life cycle, and its conditional depletion offers a method to study the sexual development of the parasite in vitro, and is proposed as an alternative to the requirement of T. gondii infections in cats.</p>',
			'date' => '2020-02-24',
			'pmid' => 'http://www.pubmed.gov/32094587',
			'doi' => '10.1038/s41564-020-0674-4',
			'modified' => '2020-03-20 17:27:25',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3866',
			'name' => 'Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome.',
			'authors' => 'Cooper A, Butto T, Hammer N, Jagannath S, Fend-Guella DL, Akhtar J, Radyushkin K, Lesage F, Winter J, Strand S, Roeper J, Zechner U, Schweiger S',
			'description' => '<p>Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an imprinting disorder.</p>',
			'date' => '2020-01-24',
			'pmid' => 'http://www.pubmed.gov/31980599',
			'doi' => '10.1038/s41467-019-13918-4',
			'modified' => '2020-03-20 17:50:11',
			'created' => '2020-03-13 13:45:54',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3802',
			'name' => 'Analysis of Histone Modifications in Rodent Pancreatic Islets by Native Chromatin Immunoprecipitation.',
			'authors' => 'Sandovici I, Nicholas LM, O'Neill LP',
			'description' => '<p>The islets of Langerhans are clusters of cells dispersed throughout the pancreas that produce several hormones essential for controlling a variety of metabolic processes, including glucose homeostasis and lipid metabolism. Studying the transcriptional control of pancreatic islet cells has important implications for understanding the mechanisms that control their normal development, as well as the pathogenesis of metabolic diseases such as diabetes. Histones represent the main protein components of the chromatin and undergo diverse covalent modifications that are very important for gene regulation. Here we describe the isolation of pancreatic islets from rodents and subsequently outline the methods used to immunoprecipitate and analyze the native chromatin obtained from these cells.</p>',
			'date' => '2020-01-01',
			'pmid' => 'http://www.pubmed.gov/31586329',
			'doi' => '10.1007/978-1-4939-9882-1',
			'modified' => '2019-12-05 11:28:01',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3838',
			'name' => 'Unraveling the role of H3K4 trimethylation and lncRNA HOTAIR in SATB1 and DUSP4-dependent survival of virulent Mycobacterium tuberculosis in macrophages',
			'authors' => 'Subuddhi Arijita, Kumar Manish, Majumder Debayan, Sarkar Arijita, Ghosh Zhumur, Vasudevan Madavan, Kundu Manikuntala, Basu Joyoti',
			'description' => '<p>The modification of chromatin influences host transcriptional programs during bacterial infection, at times skewing the balance in favor of pathogen survival. To test the role of chromatin modifications during Mycobacterium tuberculosis infection, we analysed genome-wide deposition of H3K4me3 marks in macrophages infected with either avirulent M. tuberculosis H37Ra or virulent H37Rv, by chromatin immunoprecipitation, followed by sequencing. We validated differences in association of H3K4me3 at the loci of special AT-rich sequence binding protein 1 (SATB1) and dual specificity MAP kinase phosphatase 4 (DUSP4) between H37Rv and H37Ra-infected macrophages, and demonstrated their role in regulating bacterial survival in macrophages as well as the expression of chemokines. SATB1 repressed gp91phox (an NADPH oxidase subunit) thereby regulating reactive oxygen species (ROS) generation during infection. Long non-coding RNA HOX transcript antisense RNA (HOTAIR) was upregulated in H37Ra-, but downregulated in H37Rv-infected macrophages. HOTAIR overexpression correlated with deposition of repressive H3K27me3 marks around the TSSs of DUSP4 and SATB1, suggesting that its downregulation favors the transcription of SATB1 and DUSP4. In summary, we have delineated histone modification- and lncRNA-dependent mechanisms regulating gene expression patterns facilitating survival of virulent M. tuberculosis. Our observations raise the possibility of harnessing histone-modifying enzymes to develop host-directed therapies for tuberculosis.</p>',
			'date' => '2019-12-22',
			'pmid' => 'https://doi.org/10.1016/j.tube.2019.101897',
			'doi' => '10.1016/j.tube.2019.101897',
			'modified' => '2020-02-20 11:22:43',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3807',
			'name' => 'Epigenetic remodelling licences adult cholangiocytes for organoid formation and liver regeneration.',
			'authors' => 'Aloia L, McKie MA, Vernaz G, Cordero-Espinoza L, Aleksieva N, van den Ameele J, Antonica F, Font-Cunill B, Raven A, Aiese Cigliano R, Belenguer G, Mort RL, Brand AH, Zernicka-Goetz M, Forbes SJ, Miska EA, Huch M',
			'description' => '<p>Following severe or chronic liver injury, adult ductal cells (cholangiocytes) contribute to regeneration by restoring both hepatocytes and cholangiocytes. We recently showed that ductal cells clonally expand as self-renewing liver organoids that retain their differentiation capacity into both hepatocytes and ductal cells. However, the molecular mechanisms by which adult ductal-committed cells acquire cellular plasticity, initiate organoids and regenerate the damaged tissue remain largely unknown. Here, we describe that ductal cells undergo a transient, genome-wide, remodelling of their transcriptome and epigenome during organoid initiation and in vivo following tissue damage. TET1-mediated hydroxymethylation licences differentiated ductal cells to initiate organoids and activate the regenerative programme through the transcriptional regulation of stem-cell genes and regenerative pathways including the YAP-Hippo signalling. Our results argue in favour of the remodelling of genomic methylome/hydroxymethylome landscapes as a general mechanism by which differentiated cells exit a committed state in response to tissue damage.</p>',
			'date' => '2019-11-04',
			'pmid' => 'http://www.pubmed.gov/31685987',
			'doi' => '10.1038/s41556-019-0402-6',
			'modified' => '2019-12-05 11:19:34',
			'created' => '2019-12-02 15:25:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3723',
			'name' => 'Interleukin-22 protects intestinal stem cells against genotoxic stress.',
			'authors' => 'Gronke K, Hernández PP, Zimmermann J, Klose CSN, Kofoed-Branzk M, Guendel F, Witkowski M, Tizian C, Amann L, Schumacher F, Glatt H, Triantafyllopoulou A, Diefenbach A',
			'description' => '<p>Environmental genotoxic factors pose a challenge to the genomic integrity of epithelial cells at barrier surfaces that separate host organisms from the environment. They can induce mutations that, if they occur in epithelial stem cells, contribute to malignant transformation and cancer development. Genome integrity in epithelial stem cells is maintained by an evolutionarily conserved cellular response pathway, the DNA damage response (DDR). The DDR culminates in either transient cell-cycle arrest and DNA repair or elimination of damaged cells by apoptosis. Here we show that the cytokine interleukin-22 (IL-22), produced by group 3 innate lymphoid cells (ILC3) and &gamma;&delta; T cells, is an important regulator of the DDR machinery in intestinal epithelial stem cells. Using a new mouse model that enables sporadic inactivation of the IL-22 receptor in colon epithelial stem cells, we demonstrate that IL-22 is required for effective initiation of the DDR following DNA damage. Stem cells deprived of IL-22 signals and exposed to carcinogens escaped DDR-controlled apoptosis, contained more mutations and were more likely to give rise to colon cancer. We identified metabolites of glucosinolates, a group of phytochemicals contained in cruciferous vegetables, to be a widespread source of genotoxic stress in intestinal epithelial cells. These metabolites are ligands of the aryl hydrocarbon receptor (AhR), and AhR-mediated signalling in ILC3 and &gamma;&delta; T cells controlled their production of IL-22. Mice fed with diets depleted of glucosinolates produced only very low levels of IL-22 and, consequently, the DDR in epithelial cells of mice on a glucosinolate-free diet was impaired. This work identifies a homeostatic network protecting stem cells against challenge to their genome integrity by AhR-mediated 'sensing' of genotoxic compounds from the diet. AhR signalling, in turn, ensures on-demand production of IL-22 by innate lymphocytes directly regulating components of the DDR in epithelial stem cells.</p>',
			'date' => '2019-02-01',
			'pmid' => 'http://www.pubmed.gov/30700914',
			'doi' => '10.1038/s41586-019-0899-7',
			'modified' => '2019-08-07 10:28:18',
			'created' => '2019-07-31 13:35:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '3500',
			'name' => 'H3K4/K9 acetylation and Lr28-mediated expression of six leaf rust responsive genes in wheat (Triticum aestivum).',
			'authors' => 'Sharma C, Kumar S, Saripalli G, Jain N, Raghuvanshi S, Sharma JB, Prabhu KV, Sharma PK, Balyan HS, Gupta PK',
			'description' => '<p>Development of leaf rust-resistant cultivars is a priority during wheat breeding, since leaf rust causes major losses in yield. Resistance against leaf rust due to Lr genes is partly controlled by epigenetic modifications including histone acetylation that is known to respond to biotic/abiotic stresses. In the present study, enrichment of H3K4ac and H3K9ac in promoters of six defense responsive genes (N-acetyltransferase, WRKY 40, WRKY 70, ASR1, Peroxidase 12 and Sarcosine oxidase) was compared with their expression in a pair of near-isogenic lines (NILs) for the gene Lr28 following inoculation with leaf rust pathotype '77-5'; ChIP-qPCR was used for this purpose. The proximal and distal promoters of these genes contained a number of motifs that are known to respond to biotic stresses. The enrichment of two acetylation marks changed with passage of time; changes in expression of two of the six genes (N-acetyltransferase and peroxidase12), largely matched with changes in H3K4/H3K9 acetylation patterns of the two promoter regions. For example, enrichment of both the marks matched with higher expression of N-acetyltransferase gene in susceptible NIL and the deacetylation (H3K4ac) largely matched with reduced gene expression in resistant NIL. In peroxidase12, enrichment of H3K4ac and H3K9ac largely matched with higher expression in both the NILs. In the remaining four genes, changes in H3 acetylation did not always match with gene expression levels. This indicated complexity in the regulation of the expression of these remaining four genes, which may be controlled by other epigenetic/genetic regulatory mechanisms that need further analysis.</p>',
			'date' => '2018-10-08',
			'pmid' => 'http://www.pubmed.org/30298213',
			'doi' => '10.1007/s00438-018-1500-z',
			'modified' => '2019-02-27 16:25:07',
			'created' => '2019-02-27 12:54:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3407',
			'name' => 'The histone demethylase Jarid1b mediates angiotensin II-induced endothelial dysfunction by controlling the 3'UTR of soluble epoxide hydrolase.',
			'authors' => 'Vasconez AE, Janetzko P, Oo JA, Pflüger-Müller B, Ratiu C, Gu L, Helin K, Geisslinger G, Fleming I, Schröder K, Fork C, Brandes RP, Leisegang MS',
			'description' => '<p>AIM: The histone demethylase Jarid1b limits gene expression by removing the active methyl mark from histone3 lysine4 at gene promoter regions. A vascular function of Jarid1b is unknown, but a vasoprotective function to inflammatory and hypertrophic stimuli, like angiotensin II (AngII) could be inferred. This hypothesis was tested using Jarid1b knockout mice and the inhibitor PBIT. METHODS: Mice or aortic segments were treated with AngII to induce endothelial dysfunction. Aortae from WT and Jarid1b knockout were studied in organ chambers and endothelium-dependent dilator responses to acetylcholine and endothelium-independent responses to DetaNONOate were recorded after pre-constriction with phenylephrine in the presence or absence of the NO-synthase inhibitor nitro-L-arginine. Molecular mechanisms were investigated with chromatin immunoprecipitation, RNA-Seq, RNA-3'-adaptor-ligation, actinomycin D and RNA-immunoprecipitation. RESULTS: Knockout or inhibition of Jarid1b prevented the development of endothelial dysfunction in response to AngII. This effect was not a consequence of altered nitrite oxide availability but accompanied by a loss of the inflammatory response to AngII. As Jarid1b mainly inhibits gene expression, an indirect effect should account for this observation. AngII induced the soluble epoxide hydrolase (sEH), which degrades anti-inflammatory lipids, and thus promotes inflammation. Knockout or inhibition of Jarid1b prevented the AngII-mediated sEH induction. Mechanistically, Jarid1b maintained the length of the 3'untranslated region of the sEH mRNA, thereby increasing its stability and thus sEH protein expression. Loss of Jarid1b activity therefore resulted in sEH mRNA destabilization. CONCLUSION: Jarid1b contributes to the pro-inflammatory effects of AngII by stabilizing sEH expression. Jarid1b inhibition might be an option for future therapeutics against cardiovascular dysfunction.</p>',
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			'description' => '<p>Innate immune cells can develop long-term memory after stimulation by microbial products during infections or vaccinations. Here, we report that metabolic signals can induce trained immunity. Pharmacological and genetic experiments reveal that activation of the cholesterol synthesis pathway, but not the synthesis of cholesterol itself, is essential for training of myeloid cells. Rather, the metabolite mevalonate is the mediator of training via activation of IGF1-R and mTOR and subsequent histone modifications in inflammatory pathways. Statins, which block mevalonate generation, prevent trained immunity induction. Furthermore, monocytes of patients with hyper immunoglobulin D syndrome (HIDS), who are mevalonate kinase deficient and accumulate mevalonate, have a constitutive trained immunity phenotype at both immunological and epigenetic levels, which could explain the attacks of sterile inflammation that these patients experience. Unraveling the role of mevalonate in trained immunity contributes to our understanding of the pathophysiology of HIDS and identifies novel therapeutic targets for clinical conditions with excessive activation of trained immunity.</p>',
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	)
)
$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/27902686" 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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