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Key Documents

ABE1867

Sigma-Aldrich

Anti-MLL4 Antibody

from rabbit, purified by affinity chromatography

Sinónimos:

Histone-lysine N-methyltransferase 2D, ALL1-related protein, Lysine N-methyltransferase 2D, Myeloid/lymphoid or mixed-lineage leukemia protein 2

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About This Item

UNSPSC Code:
12352203
eCl@ss:
32160702

biological source

rabbit

Quality Level

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

purified by

affinity chromatography

species reactivity

human, mouse

technique(s)

ChIP: suitable (ChIP-seq)
western blot: suitable

NCBI accession no.

UniProt accession no.

shipped in

ambient

target post-translational modification

unmodified

Gene Information

human ... KMT2D(8085)

General description

Histone-lysine N-methyltransferase 2D (EC 2.1.1.43; UniProt O14686; also known as MLL4, ALL1-related protein, Lysine N-methyltransferase 2D) is encoded by the KMT2D (also known as MLL4, ALR, KABUK1, MLL2) gene (Gene ID: 8085) in human. MLL4 methylates Lys-4 of histone H3 to form H3K4 mono- and di-methylation (H3K4me1/2), which represents a specific tag for transcriptional enhancers. MLL4 is also a component of the MLL3/4 protein complex that plays an important role during cell differentiation and animal development. MLL4 is localized to the nucleus and is expressed in most embryonic and adult tissues. Defects in MLL4 (often known as KMT2D in the literature) have been linked to Kabuki syndrome and congenital heart diseases. Inactivating mutations in MLL4/MLL2/KMT2D gene have been linked to many types of cancers, including medulloblastoma, non-Hodgkin lymphoma, diffuse large B-cell lymphoma, prostate cancer, breast cancer, hepatocellular carcinoma, ovarian cancer, lung, bladder, head & neck cancers, and pancreatic cancer. (Ref.: Lee, J.E., et al. (2013). Elife. 2:e01503; Lawrence, M.S., et al., (2014). Nature. 505(7484):495-501).

Specificity

This polyclonal antibody targets the region between the first and third coiled coil of MLL4 sequence.

Immunogen

Epitope: unknown
His-tagged recombinant human MLL4 internal fragment from the region between the first and third coiled coil.

Application

Anti-MLL4, Cat. No. ABE1867, is a highly specific rabbit polyclonal antibody that targets MLL4 (also known as KMT2D) and has been tested in Chromatin Immunoprecipitation (ChIP), ChIP-seq, Immunoprecipitation, and Western Blotting.
Research Category
Epigenetics & Nuclear Function
Western Blotting Analysis: A 1:500 dilution of the unpurified antiserum detected the expression of Myc-tagged human MLL4 a.a. 2916-3785, but not a.a. 3662-4625, fragment in 100 µg whole cell lysate from respective transfectants (Courtesy of Dr Lee from NIH).

Chromatin Immunoprecipitation (ChIP) Analysis: A representative lot detected MLL4 (MLL2) occupancy on the PPAR 1, but not the PPAR 2, proximal promoter in MEFs, while MLL4 enrichment was found on PPARγ1, PPARγ2, and C/EBP promoters in differentiating murine brown preadipocytes (Cho, Y.W., et al. (2009). Cell Metab. 10(1):27-39).

ChIP-Sequencing (ChIP-seq) Analysis: A representative lot detected MLL4 MLL4 genomic enrichment sites in a cell type- and differentiation stage-specific manner (Lee, J.E., et al. (2013). Elife. 2:e01503).

Immunoprecipitation Analysis: A representative lot immunoprecipitated MLL3/MLL4 complex components (UTX, PTIP, RbBP5 and PA1) and C/EBPβ, but not Menin, from mouse brown preadipocyte nuclear extracts prepared at day 2 of adipogenesis (Lee, J.E., et al. (2013). Elife. 2:e01503).

Quality

Evaluated by Western Blotting of recombinant MLL4 fragment.

Western Blotting Analysis: A 1:5,000 dilution of this antibody detected 50 ng of recombinant human MLL4 fragment.

Target description

593.4/593.7 kDa (human isoform 1/2) and 600.2 kDa (mouse) calculated.

Physical form

Affinity purified.
Purified rabbit polyclonal antibody in buffer containing 0.1 M Tris-Glycine (pH 7.4), 150 mM NaCl with 0.05% sodium azide.

Storage and Stability

Stable for 1 year at 2-8°C from date of receipt.

Other Notes

Concentration: Please refer to lot specific datasheet.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class

12 - Non Combustible Liquids

wgk_germany

WGK 1


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Wei Liu et al.
Cancer biology & therapy, 24(1), 2216041-2216041 (2023-06-08)
Pancreatic adenocarcinoma (PAAD) is a major cause of mortality related to cancer worldwide. This paper dissected the functions of the CSTF2T/ASH2L/CALB2 axis in PAAD progression. CALB2 expression was assessed in PAAD tissues and cells using RT-qPCR and western blot. Subsequent
Xinmiao Wang et al.
Cell & bioscience, 12(1), 49-49 (2022-04-29)
Epigenetic reprogramming is involved in multiple steps of human cancer evolution and is mediated by a variety of chromatin-modifying enzymes. Specifically, the histone lysine methyltransferase KMT2D is among the most frequently mutated genes in oral squamous cell carcinoma (OSCC). However
Balkees Abderrahman et al.
Molecular cancer therapeutics, 20(1), 11-25 (2020-11-13)
Patients with long-term estrogen-deprived breast cancer, after resistance to tamoxifen or aromatase inhibitors develops, can experience tumor regression when treated with estrogens. Estrogen's antitumor effect is attributed to apoptosis via the estrogen receptor (ER). Estrogen treatment can have unpleasant gynecologic
Jill A Fahrner et al.
JCI insight, 4(20) (2019-09-27)
Kabuki syndrome 1 (KS1) is a Mendelian disorder of the epigenetic machinery caused by mutations in the gene encoding KMT2D, which methylates lysine 4 on histone H3 (H3K4). KS1 is characterized by intellectual disability, postnatal growth retardation, and distinct craniofacial
Jie Li et al.
Nature communications, 15(1), 2879-2879 (2024-04-04)
Despite regulating overlapping gene enhancers and pathways, CREBBP and KMT2D mutations recurrently co-occur in germinal center (GC) B cell-derived lymphomas, suggesting potential oncogenic cooperation. Herein, we report that combined haploinsufficiency of Crebbp and Kmt2d induces a more severe mouse lymphoma

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