High Quality Antibodies for Epigenetics▸

Featured Epigenetic Antibody: 5-Methylcytosine▸

Epigenetics Interactive Histone Modification Pathway▸

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High Quality Antibodies for Epigenetics

Epigenetics is the study of phenotypical changes which occur via mechanisms other than DNA sequence alteration.  These changes are mediated by the covalent attachment of chemical groups to DNA and its associated proteins, histones and chromatin.  Types of epigenetic modification include:  ADP-ribosylation, acetylation, methylation, phosphorylation, sumoylation and ubiquitination (1).   

Rabbit Monoclonal Antibodies (RabMAbs) are ideal tool for detecting these epigenetic modifications.  The rabbit immune system has a much better response to small epitopes than the mouse immune system, allowing the development of high quality antibody to subtle changes in epitopes such as post-translational modifications and activations (2,3). Additionally, RabMAbs offer high affinity and specificity to the modified target with minimal cross-reactivity to the non-modified site.

We have now generated more than 500 modification-specific and activation-specific antibodies using our patented technology.
Additionally, every Epitomics RabMAb is validated in western blot, immunohistochemistry, immunofluorescence, immunoprecipitation and flow cytometry before release, so you can be assured for which assays the antibody will work in.

See the complete list of antibodies for Epigenetics ▸

Complete list of Epigenetic Antibodies

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Featured Epigenetic Antibody: 5-Methylcytosine RabMAb

In higher eukaryotes, one of the key epigenetic events, DNA methylation, has been identified as being involved in gene regulation, genomic imprinting, carcinogenesis, X-chromosome inactivation, aging, and suppression of repetitive elements.    In mammalian cells, DNA methylation is an enzymatic modification at the 5-position of cytosine and is abundantly present within the CpG dinucleotide sequence context.  The methylated form of cytosine is known as 5-Methylcytosine (5-hmC) or 5-Methylcytidine.

This DNA modification is inheritable and reversible without primary DNA base sequence changes resulting in possible epigenetic modulation of phenotype and gene expression. CpG methylation may directly interfere with the binding of certain transcriptional regulators to their cognate DNA sequences or may enable recruitment of methyl-CpG binding proteins that create a repressed chromatin environment. The de novo formation and maintenance of 5-methylcytosine is catalyzed by DNA methyltransferase proteins (DNMTs).  

Utilizing Rabbit Monoclonal’s ability to generate high quality antibodies to subtle changes in epitopes, Epitomics has developed a highly specific and sensitive Rabbit Monoclonal Antibody which specifically recognises 5-Methylcytosine (5-hmC).

Epitomics' 5-Methylcytosine (5-hmC) RabMAb, clone EP4694, has been validated for use in ELISA, ICC (IF) and MeDIP / mDIP applications.

	Competitive ELISA: 0.1 ug/ml of BSA-methylcytosine was coated into 96-wells. 5 mg/ml of competitor's methylcytosine, cytosine, or hydroxymethylcytosine and 0.1 ug/ml of anti-5-Methylcytosine antibody (cat.# 3913-1) were added. HRP conjugated goat anti-rabbit IgG antibody was used to develop the color.
MeDIP using 5-mC RabMAb (Cat# 3913-1) on Jurkat genomic DNA (4ug) and fully methylated Jurkat DNA (0.5ug). BRCA1 primer was used for PCR. A. DNA Ladder (1-100 bp) B. Jurkat genomic DNA + Rabbit IgG C. Jurkat genomic DNA + 5-mC RabMAb D. Methlyated Jurkat DNA + 5-mC RabMAb	Catalog #3913-1 Applications: MeDIP, ICC, ELISA Species: Human, Mouse, Rat Product Page

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References

1. Epigenetic signatures of stem-cell identity Mikhail Spivakov and Amanda G. Fisher, Nature Reviews Genetics 8, 263-271 (April 2007)
2. A humanized anti-VEGF rabbit monoclonal antibody inhibits angiogenesis and blocks tumor growth in xenograft models Yu Y, et al., [PLoS One. 2010 Feb 5;5(2):e9072]
3. Rabbit monoclonal antibody: potential application in cancer therapy Lifeng Feng, Xian Wang, and Hongchuan Jin [Am J Transl Res. 2011 May 15; 3(3): 269–274]