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Mll4 antibody

CUT&Tag grade Abs

ChIP-seq grade Abs

ChIP grade Abs

Negative IgG control

Antibody portal

Antibodies

Catalog Number

Format

Price

C15310100
(CS-100-100)

100 µl

$260.00
Bulk order

Other format

C15310100-20

20 µl

Alternative names: ALR, MLL2, Kmt2d

Polyclonal antibody raised in rabbit against mouse Mll4 (Myeloid/lymphoid or mixed-lineage leukemia protein 4), using three KLH-conjugated synthetic peptides containing an amino acid sequence from the central part of the protein.

Lot	A274-001
Concentration	not determined
Species reactivity	Mouse: positive. Other species: not tested.
Type	Polyclonal
Purity	Whole antiserum
Host	Rabbit
Storage Conditions	Store at -20°C; for long storage, store at -80°C. Avoid multiple freeze-thaw cycles.
Precautions	This product is for research use only. Not for use in diagnostic or therapeutic procedures.

Applications	Suggested dilution	References
ELISA	1:1,000 - 1:5,000	Fig 1
Western Blotting	1:500	Fig 2, (1)

Validation Data

Figure 1. Determination of the titer
To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against mouse Mll4 (cat. No. C15310100). The wells were coated with the peptides used for immunisation of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:54,000.

Figure 2. Western blot analysis using the Diagenode antibody directed against Mll4 (1)
Western blot was performed on whole cell lysates from mouse embryonic stem cells (E14Tg2a) with the Diagenode antibody against mouse Mll4 (ca. No. C15310100), diluted 1:500 in PBS-Tween containing 5% skimmed milk. The location of the protein of interest (~ 600 kDa) is indicated on the right; the location of the 500 kDa MW marker is shown on the left. Cells homozygous for the targeted mll4 allele (-/-) show a complete loss of Mll4 protein, whereas the Mll4 protein was detected in flp-recombined ES cells (F/F) and heterozygously targeted ES cells (+/-).
Target description
Mll4 (UniProtKB/Swiss-Prot entry O14686) is involved in the methylation of lys 4 of histone H3, thus acting as a transcriptional
regulator.

Publications

How to properly cite this product in your work

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Using our products in your publication? Let us know!

KMT2D deficiency drives lung squamous cell carcinoma andhypersensitivity to RTK-RAS inhibition.
Pan Yuanwang et al.
Lung squamous cell carcinoma (LUSC) represents a major subtype of lung cancer with limited treatment options. KMT2D is one of the most frequently mutated genes in LUSC (>20\%), and yet its role in LUSC oncogenesis remains unknown. Here, we identify KMT2D as a key regulator of LUSC tumorigenesis wherein Kmt2d dele...

Mll3 and Mll4 Facilitate Enhancer RNA Synthesis and Transcription from Promoters Independently of H3K4 Monomethylation
Doroghi K.M. et al.
Monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation of histone H3 at lysine 27 (H3K27ac) are correlated with transcriptionally engaged enhancer elements, but the functional impact of these modifications on enhancer activity is not well understood. Here we used CRISPR/Cas9 genome editing to ...

Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis
Zhang J, Dominguez-Sola D, Hussein S, Lee JE, Holmes AB, Bansal M, Vlasevska S, Mo T, Tang H, Basso K, Ge K, Dalla-Favera R, Pasqualucci L
Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show tha...

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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
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<li>Highly sensitive and specific</li>
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			'description' => '<p>Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events.</p>',
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	'meta_title' => ' Western Blot  - Monoclonal antibody - Polyclonal antibody  | Diagenode',
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	'created' => '2015-01-07 09:20:00',
	'locale' => 'eng'
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<p><em></em>Check our selection of antibodies validated in Western blot.</p>'
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	'authors' => 'Zhang J, Dominguez-Sola D, Hussein S, Lee JE, Holmes AB, Bansal M, Vlasevska S, Mo T, Tang H, Basso K, Ge K, Dalla-Favera R, Pasqualucci L',
	'description' => '<p>Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events.</p>',
	'date' => '2015-10-01',
	'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26366712',
	'doi' => ' 10.1038/nm.3940',
	'modified' => '2016-05-11 10:19:28',
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include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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<p><small><strong>Figure 1. Determination of the titer</strong> <br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against mouse Mll4 (cat. No. C15310100). The wells were coated with the peptides used for immunisation of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:54,000.</small></p>
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<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310100_fig2.png" alt="Western blot" /></p>
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<div class="small-6 columns">
<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against Mll4 (1)</strong><br />Western blot was performed on whole cell lysates from mouse embryonic stem cells (E14Tg2a) with the Diagenode antibody against mouse Mll4 (ca. No. C15310100), diluted 1:500 in PBS-Tween containing 5% skimmed milk. The location of the protein of interest (~ 600 kDa) is indicated on the right; the location of the 500 kDa MW marker is shown on the left. Cells homozygous for the targeted mll4 allele (-/-) show a complete loss of Mll4 protein, whereas the Mll4 protein was detected in flp-recombined ES cells (F/F) and heterozygously targeted ES cells (+/-).</small></p>
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<p>Learn more about: <a href="../applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
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	'meta_title' => ' Western Blot  - Monoclonal antibody - Polyclonal antibody  | Diagenode',
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<p>Learn more about: <a href="../applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>'
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	'authors' => 'Zhang J, Dominguez-Sola D, Hussein S, Lee JE, Holmes AB, Bansal M, Vlasevska S, Mo T, Tang H, Basso K, Ge K, Dalla-Favera R, Pasqualucci L',
	'description' => '<p>Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events.</p>',
	'date' => '2015-10-01',
	'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26366712',
	'doi' => ' 10.1038/nm.3940',
	'modified' => '2016-05-11 10:19:28',
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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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		'slug' => 'mll4-polyclonal-antibody-pioneer-100-ul',
		'meta_title' => 'Mll4 Polyclonal Antibody | Diagenode',
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		'meta_description' => 'Mll4 (Myeloid/lymphoid or mixed-lineage leukemia protein 4) Polyclonal Antibody validated  in ELISA and WB. Batch-specific data available on the website. Alternative names: ALR, MLL2, Kmt2d',
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		'host' => '*****',
		'id' => '296',
		'name' => 'Mll4 polyclonal antibody',
		'description' => 'Mll4 (UniProtKB/Swiss-Prot entry O14686) is involved in the methylation of lys 4 of histone H3, thus acting as a transcriptional regulator.',
		'clonality' => '',
		'isotype' => '',
		'lot' => 'A274-001',
		'concentration' => 'not determined',
		'reactivity' => 'Mouse: positive. Other species: not tested.',
		'type' => 'Polyclonal',
		'purity' => 'Whole antiserum',
		'classification' => 'Pioneer',
		'application_table' => '<table>
<thead>
<tr>
<th>Applications</th>
<th>Suggested dilution</th>
<th>References</th>
</tr>
</thead>
<tbody>
<tr>
<td>ELISA</td>
<td>1:1,000 - 1:5,000</td>
<td>Fig 1</td>
</tr>
<tr>
<td>Western Blotting</td>
<td>1:500</td>
<td>Fig 2, (1)</td>
</tr>
</tbody>
</table>',
		'storage_conditions' => 'Store at -20°C; for long storage, store at -80°C. Avoid multiple freeze-thaw cycles.',
		'storage_buffer' => '',
		'precautions' => 'This product is for research use only. Not for use in diagnostic or therapeutic procedures.',
		'uniprot_acc' => '',
		'slug' => '',
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		'meta_description' => '',
		'modified' => '2022-01-05 11:23:14',
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			'description' => '<p><span>Alternative names: <strong>ALR</strong>, <strong>MLL2, Kmt2d<br /></strong></span></p>
<p><span>Polyclonal antibody raised in rabbit against mouse Mll4 (Myeloid/lymphoid or mixed-lineage leukemia protein 4), using three KLH-conjugated synthetic peptides containing an amino acid sequence from the central part of the protein.</span></p>',
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<div class="small-6 columns">
<p><img src="https://www.diagenode.com/img/product/antibodies/C15310100_fig1.png" alt="ELISA" /><br /><br /></p>
</div>
<div class="small-6 columns">
<p><small><strong>Figure 1. Determination of the titer</strong> <br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against mouse Mll4 (cat. No. C15310100). The wells were coated with the peptides used for immunisation of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:54,000.</small></p>
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</div>
<div class="row">
<div class="small-6 columns">
<p class="text-center"><img src="https://www.diagenode.com/img/product/antibodies/C15310100_fig2.png" alt="Western blot" /></p>
</div>
<div class="small-6 columns">
<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against Mll4 (1)</strong><br />Western blot was performed on whole cell lysates from mouse embryonic stem cells (E14Tg2a) with the Diagenode antibody against mouse Mll4 (ca. No. C15310100), diluted 1:500 in PBS-Tween containing 5% skimmed milk. The location of the protein of interest (~ 600 kDa) is indicated on the right; the location of the 500 kDa MW marker is shown on the left. Cells homozygous for the targeted mll4 allele (-/-) show a complete loss of Mll4 protein, whereas the Mll4 protein was detected in flp-recombined ES cells (F/F) and heterozygously targeted ES cells (+/-).</small></p>
</div>
</div>',
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			'description' => '<p><strong>Western blot</strong> : The quality of antibodies used in this technique is crucial for correct and specific protein identification. Diagenode offers huge selection of highly sensitive and specific western blot-validated antibodies.</p>
<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
<p><em></em>Check our selection of antibodies validated in Western blot.</p>',
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<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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			'description' => '<p><span style="font-weight: 400;">All Diagenode&rsquo;s antibodies are listed below. Please, use our Quick search field to find the antibody of interest by target name, application, purity.</span></p>
<p><span style="font-weight: 400;">Diagenode&rsquo;s highly validated antibodies:</span></p>
<ul>
<li>Highly sensitive and specific</li>
<li>Cost-effective (requires less antibody per reaction)</li>
<li>Batch-specific data is available on the website</li>
<li>Expert technical support</li>
<li>Sample sizes available</li>
<li>100% satisfaction guarantee</li>
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			'name' => 'Datasheet Mll4 C15310100',
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			'description' => '<p style="text-align: justify;"><span>Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of large sets of genome-wide sequencing data. ChIP sequencing (ChIP-seq) has now become the gold standard method for chromatin studies, given the accuracy and coverage scale of the approach over other methods. Successful ChIP-seq, however, requires a higher level of experimental accuracy and consistency in all steps of ChIP than ever before. Particularly crucial is the quality of ChIP antibodies. </span></p>',
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			'name' => 'KMT2D deficiency drives lung squamous cell carcinoma andhypersensitivity to RTK-RAS inhibition.',
			'authors' => 'Pan  Yuanwang et al.',
			'description' => '<p>Lung squamous cell carcinoma (LUSC) represents a major subtype of lung cancer with limited treatment options. KMT2D is one of the most frequently mutated genes in LUSC (&gt;20\%), and yet its role in LUSC oncogenesis remains unknown. Here, we identify KMT2D as a key regulator of LUSC tumorigenesis wherein Kmt2d deletion transforms lung basal cell organoids to LUSC. Kmt2d loss increases activation of receptor tyrosine kinases (RTKs), EGFR and ERBB2, partly through reprogramming the chromatin landscape to repress the expression of protein tyrosine phosphatases. These events provoke a robust elevation in the oncogenic RTK-RAS signaling. Combining SHP2 inhibitor SHP099 and pan-ERBB inhibitor afatinib inhibits lung tumor growth in Kmt2d-deficient LUSC murine models and in patient-derived xenografts (PDXs) harboring KMT2D mutations. Our study identifies KMT2D as a pivotal epigenetic modulator for LUSC oncogenesis and suggests that KMT2D loss renders LUSC therapeutically vulnerable to RTK-RAS inhibition.</p>',
			'date' => '2022-12-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36525973',
			'doi' => '10.1016/j.ccell.2022.11.015',
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			'id' => '3206',
			'name' => 'Mll3 and Mll4 Facilitate Enhancer RNA Synthesis and Transcription from Promoters Independently of H3K4 Monomethylation',
			'authors' => 'Doroghi K.M. et al.',
			'description' => '<p>Monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation of histone H3 at lysine 27 (H3K27ac) are correlated with transcriptionally engaged enhancer elements, but the functional impact of these modifications on enhancer activity is&nbsp;not well understood. Here we used CRISPR/Cas9&nbsp;genome editing to separate catalytic activity-dependent and independent functions of Mll3 (Kmt2c) and Mll4 (Kmt2d, Mll2), the major enhancer H3K4 monomethyltransferases. Loss of H3K4me1 from enhancers in Mll3/4 catalytically deficient cells causes partial reduction of H3K27ac, but has surprisingly minor effects on transcription from either enhancers or promoters. In contrast, loss of Mll3/4 proteins leads to strong depletion of enhancer Pol&nbsp;II occupancy and eRNA synthesis, concomitant with downregulation of target genes. Interestingly, downregulated genes exhibit reduced polymerase levels in gene bodies, but not at promoters, suggestive of pause-release defects. Altogether, our results suggest that enhancer H3K4me1 provides only a minor contribution to the long-range coactivator function of Mll3/4.</p>',
			'date' => '2017-05-18',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28483418',
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			'name' => 'Disruption of KMT2D perturbs germinal center B cell development and promotes lymphomagenesis',
			'authors' => 'Zhang J, Dominguez-Sola D, Hussein S, Lee JE, Holmes AB, Bansal M, Vlasevska S, Mo T, Tang H, Basso K, Ge K, Dalla-Favera R, Pasqualucci L',
			'description' => '<p>Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events.</p>',
			'date' => '2015-10-01',
			'pmid' => 'http://www.ncbi.nlm.nih.gov/pubmed/26366712',
			'doi' => ' 10.1038/nm.3940',
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
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<p>Learn more about: <a href="../applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
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<p><em></em>Check our selection of antibodies validated in Western blot.</p>'
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	'authors' => 'Zhang J, Dominguez-Sola D, Hussein S, Lee JE, Holmes AB, Bansal M, Vlasevska S, Mo T, Tang H, Basso K, Ge K, Dalla-Favera R, Pasqualucci L',
	'description' => '<p>Mutations in the gene encoding the KMT2D (or MLL2) methyltransferase are highly recurrent and occur early during tumorigenesis in diffuse large B cell lymphoma (DLBCL) and follicular lymphoma (FL). However, the functional consequences of these mutations and their role in lymphomagenesis are unknown. Here we show that FL- and DLBCL-associated KMT2D mutations impair KMT2D enzymatic activity, leading to diminished global H3K4 methylation in germinal-center (GC) B cells and DLBCL cells. Conditional deletion of Kmt2d early during B cell development, but not after initiation of the GC reaction, results in an increase in GC B cells and enhances B cell proliferation in mice. Moreover, genetic ablation of Kmt2d in mice overexpressing Bcl2 increases the incidence of GC-derived lymphomas resembling human tumors. These findings suggest that KMT2D acts as a tumor suppressor gene whose early loss facilitates lymphomagenesis by remodeling the epigenetic landscape of the cancer precursor cells. Eradication of KMT2D-deficient cells may thus represent a rational therapeutic approach for targeting early tumorigenic events.</p>',
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include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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<p><span>Polyclonal antibody raised in rabbit against mouse Mll4 (Myeloid/lymphoid or mixed-lineage leukemia protein 4), using three KLH-conjugated synthetic peptides containing an amino acid sequence from the central part of the protein.</span></p>',
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<p><img src="https://www.diagenode.com/img/product/antibodies/C15310100_fig1.png" alt="ELISA" /><br /><br /></p>
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<p><small><strong>Figure 1. Determination of the titer</strong> <br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against mouse Mll4 (cat. No. C15310100). The wells were coated with the peptides used for immunisation of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:54,000.</small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against Mll4 (1)</strong><br />Western blot was performed on whole cell lysates from mouse embryonic stem cells (E14Tg2a) with the Diagenode antibody against mouse Mll4 (ca. No. C15310100), diluted 1:500 in PBS-Tween containing 5% skimmed milk. The location of the protein of interest (~ 600 kDa) is indicated on the right; the location of the 500 kDa MW marker is shown on the left. Cells homozygous for the targeted mll4 allele (-/-) show a complete loss of Mll4 protein, whereas the Mll4 protein was detected in flp-recombined ES cells (F/F) and heterozygously targeted ES cells (+/-).</small></p>
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<td>1:1,000 - 1:5,000</td>
<td>Fig 1</td>
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<td>Western Blotting</td>
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<td>Fig 2, (1)</td>
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<p><small><strong>Figure 1. Determination of the titer</strong> <br />To determine the titer, an ELISA was performed using a serial dilution of the Diagenode antibody directed against mouse Mll4 (cat. No. C15310100). The wells were coated with the peptides used for immunisation of the rabbit. By plotting the absorbance against the antibody dilution (Figure 1), the titer of the antibody was estimated to be 1:54,000.</small></p>
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<p><small><strong>Figure 2. Western blot analysis using the Diagenode antibody directed against Mll4 (1)</strong><br />Western blot was performed on whole cell lysates from mouse embryonic stem cells (E14Tg2a) with the Diagenode antibody against mouse Mll4 (ca. No. C15310100), diluted 1:500 in PBS-Tween containing 5% skimmed milk. The location of the protein of interest (~ 600 kDa) is indicated on the right; the location of the 500 kDa MW marker is shown on the left. Cells homozygous for the targeted mll4 allele (-/-) show a complete loss of Mll4 protein, whereas the Mll4 protein was detected in flp-recombined ES cells (F/F) and heterozygously targeted ES cells (+/-).</small></p>
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<p>Learn more about: <a href="https://www.diagenode.com/applications/western-blot">Loading control, MW marker visualization</a><em>. <br /></em></p>
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			'name' => 'KMT2D deficiency drives lung squamous cell carcinoma andhypersensitivity to RTK-RAS inhibition.',
			'authors' => 'Pan  Yuanwang et al.',
			'description' => '<p>Lung squamous cell carcinoma (LUSC) represents a major subtype of lung cancer with limited treatment options. KMT2D is one of the most frequently mutated genes in LUSC (&gt;20\%), and yet its role in LUSC oncogenesis remains unknown. Here, we identify KMT2D as a key regulator of LUSC tumorigenesis wherein Kmt2d deletion transforms lung basal cell organoids to LUSC. Kmt2d loss increases activation of receptor tyrosine kinases (RTKs), EGFR and ERBB2, partly through reprogramming the chromatin landscape to repress the expression of protein tyrosine phosphatases. These events provoke a robust elevation in the oncogenic RTK-RAS signaling. Combining SHP2 inhibitor SHP099 and pan-ERBB inhibitor afatinib inhibits lung tumor growth in Kmt2d-deficient LUSC murine models and in patient-derived xenografts (PDXs) harboring KMT2D mutations. Our study identifies KMT2D as a pivotal epigenetic modulator for LUSC oncogenesis and suggests that KMT2D loss renders LUSC therapeutically vulnerable to RTK-RAS inhibition.</p>',
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			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36525973',
			'doi' => '10.1016/j.ccell.2022.11.015',
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			'name' => 'Mll3 and Mll4 Facilitate Enhancer RNA Synthesis and Transcription from Promoters Independently of H3K4 Monomethylation',
			'authors' => 'Doroghi K.M. et al.',
			'description' => '<p>Monomethylation of histone H3 at lysine 4 (H3K4me1) and acetylation of histone H3 at lysine 27 (H3K27ac) are correlated with transcriptionally engaged enhancer elements, but the functional impact of these modifications on enhancer activity is&nbsp;not well understood. Here we used CRISPR/Cas9&nbsp;genome editing to separate catalytic activity-dependent and independent functions of Mll3 (Kmt2c) and Mll4 (Kmt2d, Mll2), the major enhancer H3K4 monomethyltransferases. Loss of H3K4me1 from enhancers in Mll3/4 catalytically deficient cells causes partial reduction of H3K27ac, but has surprisingly minor effects on transcription from either enhancers or promoters. In contrast, loss of Mll3/4 proteins leads to strong depletion of enhancer Pol&nbsp;II occupancy and eRNA synthesis, concomitant with downregulation of target genes. Interestingly, downregulated genes exhibit reduced polymerase levels in gene bodies, but not at promoters, suggestive of pause-release defects. Altogether, our results suggest that enhancer H3K4me1 provides only a minor contribution to the long-range coactivator function of Mll3/4.</p>',
			'date' => '2017-05-18',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28483418',
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Datasheet Mll4 C15310100 DATASHEET Polyclonal antibody raised in rabbit against mouse Mll4 (Myeloid/lymphoid or mixed-lineage leukem...	Download
Antibodies you can trust POSTER Epigenetic research tools have evolved over time from endpoint PCR to qPCR to the analyses of lar...	Download
Epigenetic Antibodies Brochure BROCHURE More than in any other immuoprecipitation assays, quality antibodies are critical tools in many e...	Download

SDS C15310100 MLL4 Antibody GB en	Download
SDS C15310100 MLL4 Antibody US en	Download
SDS C15310100 MLL4 Antibody DE de	Download
SDS C15310100 MLL4 Antibody JP ja	Download
SDS C15310100 MLL4 Antibody BE nl	Download
SDS C15310100 MLL4 Antibody BE fr	Download
SDS C15310100 MLL4 Antibody FR fr	Download
SDS C15310100 MLL4 Antibody ES es	Download