Product Name
Anti-trimethyl-Histone H3 (Lys9) Antibody, clone 6F12-H4, clone 6F12-H4, from mouse
biological source
mouse
antibody form
purified antibody
antibody product type
primary antibodies
clone
6F12-H4, monoclonal
species reactivity
mouse, human
technique(s)
ChIP: suitable (ChIP-seq)
dot blot: suitable
immunofluorescence: suitable
inhibition assay: suitable (peptide)
western blot: suitable
isotype
IgG1κ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
trimethylation (Lys9)
Quality Level
Gene Information
human ... H3C1(8350)
mouse ... H3C1(360198)
Analysis Note
Western Blot Analysis: A 0.5 – 5 μg dilution of this lot detected trimethyl histone H3 (Lys9) in HeLa acid extracts.
Application
Representative data from a previous lot. Sonicated 3T3 L1 chromatin was subjected to chromatin immunoprecipitation using anti- trimethyl-histone H3 (Lys9) and the Magna ChIP G (Cat. #17-611) Kit. Successful immunoprecipitation of trimethylhistone H3 (Lys9) associated DNA fragments was verified by qPCR using primers flanking the p16 promoter.
Peptide Inhibition Analysis:
Peptide blocking assay demonstrates distinct preference of the antibody for the trimethyl form vs. the dimethyl form.
Chromatin Immunoprecipitation (ChIP):
ChIP analysis of known chromosomal Suv39h targets (H3K9me3 in major satellites, mouseES cells).
Dot Blot Analysis:
Dot-blot analysis demonstrating specificity of anti-H3K9me3, clone 6F12-H4 for trimethyl Lys9 of histone H3.
Biochem/physiol Actions
General description
Physical form
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Storage Class
12 - Non Combustible Liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Related Content
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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).
Global Trade Item Number
| SKU | GTIN |
|---|---|
| 05-1242 | 04053252740237 |
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