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About This Item
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
9-12, monoclonal
species reactivity
mouse, human
manufacturer/tradename
Upstate®
technique(s)
ChIP: suitable
immunofluorescence: suitable
immunoprecipitation (IP): suitable
western blot: suitable
isotype
IgG1
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... KMT2A(4297)
General description
Immunogen
Application
Chromatin Immnuoprecipitation (ChIP) Analysis: A representative lot detected MLL occupancy at the Hoxa10 and Meis promoters in mouse MLL-AF10 leukemia cells (Gallo, M., et al. (2013). Cancer Res. 73(1):417-427).
Chromatin Immnuoprecipitation (ChIP) Analysis: A representative lot detected an enhanced MLL occupancy at the Ink4a locus of 8-month-old than 2-month-old bEzTG mouse islets. The same age-dependent Ink4a locus enrichment was observed with H3K4me3, while the opposite trend was seen with Ezh and H3K27me3 enrichment at the same locus (Zhou, J.X., et al. (2013). J. Clin. Invest. 123(11):4849-4858).
Chromatin Immnuoprecipitation (ChIP) Analysis: A representative lot detected MLL occupancy at the HOXA10 promoter region in G179NS and G411NS human glioblastoma neural stem cells (Gallo, M., et al. (2013). Cancer Res. 73(1):417-427).
Chromatin Immnuoprecipitation (ChIP) Analysis: A representative lot detected MLL occupancy at the DNA replication origin (RD) as well as at both exon 1b and p16INK4a/p19ARF shared exon 2 in mouse embryonic fibroblast (MEF). An increased MLL enrichment at these sites was observed in senescent and Polycomb mutant MEFs (Agherbi, H., et al. (2009). PLoS One. 4(5):e5622).
Chromatin Immnuoprecipitation (ChIP) Analysis: A representative lot detected MLL occupancy at the Hoxa9 AB region using mouse embryonic fibroblast (MEF) chromatin preparation (Erfurth, F.E., et al. (2008). Proc. Natl. Acad. Sci. U.S.A. 105(21):7517-7522).
Immnuoprecipitation Analysis: A representative lot co-immunoprecipitated JmjD3 and RbBP5, but not Dnmt3a, with MLL from Min6 mouse insulinoma cell extract (Zhou, J.X., et al. (2013). J. Clin. Invest. 123(11):4849-4858).
Western Blotting Analysis: A representative lot detected higher MLL level in cultured glioblastoma neural stem (GNS) cells than neural stem (NS) cells, as well as MLL enrichment in the CD15+ fraction of freshly resected Glioblastoma (GBM) cells (Gallo, M., et al. (2013). Cancer Res. 73(1):417-427).
Western Blotting Analysis: A representative lot detected SET domain-containing C-terminal fragment of the MLL complex enzymatic subunit MLL (C180; MLLC) in anti-FLAG immunoprecipitate from HeLaS cells stably expressing FLAG-tagged hDPY-30 (Cho, Y.W., et al. (2007). J. Biol. Chem. 282(28):20395-20406).
Epigenetics & Nuclear Function
Histones
Biochem/physiol Actions
Physical form
Preparation Note
Analysis Note
K562 nuclear extract
Western Blotting Analysis: 0.1-1 µg/mL of this antibody detected MLL C-terminal fragment (C180; MLLC) in K562 nuclear extract.
Other Notes
Legal Information
Disclaimer
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Certificates of Analysis (COA)
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Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).
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