JMJD1B (C69G2) Rabbit mAb

3314:

Immunofluorescence , Immunoprecipitation , Western Blotting

JMJD1B (C69G2) Rabbit mAb detects endogenous levels of JMJD1B protein (all three isoforms). This antibody does not cross react with other Jumonji C proteins, including HR, JMJD1A and JMJD1C.

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the sequence of the human JMJD1B protein.

Western Blotting

Western blot analysis of extracts from HeLa and NCCIT cell lines using JMJD1B (C69G2) Rabbit mAb.

IF-IC

Confocal immunofluorescent analysis of HeLa cells using JMJD1B (C69G2) Rabbit mAb (green). Actin filaments have been labeled with DY-554 phalloidin (red).

The methylation state of lysine residues in histone proteins is a major determinant of the formation of active and inactive regions of the genome and is crucial for the proper programming of the genome during development (1,2). Jumonji C (JmjC) domain-containing proteins represent the largest class of potential histone demethylase proteins (3). The JmjC domain of several proteins has been shown to catalyze the demethylation of mono-, di-, and tri-methyl lysine residues via an oxidative reaction that requires iron and α-ketoglutarate (3). Based on homology, both humans and mice contain at least 30 such proteins, which can be divided into seven separate families (3). The JMJD1 (Jumonji domain-containing protein 1) family, also known as JHDM2 (JmjC domain-containing histone demethylation protein 2) family, contains four members: hairless (HR), JMJD1A/JHDM2A, JMJD1B/JHDM2B, and JMJD1C/JHDM2C. Hairless is expressed in the skin and brain and acts as a co-repressor of the thyroid hormone receptor (4-6). Mutations in the hairless gene cause alopecia in both mice and humans (4,5). JMJD1A is expressed in meiotic and post-meiotic male germ cells, contributes to androgen receptor-mediated gene regulation, and is required for spermatogenesis (7-9). It has also been identified as a downstream target of OCT4 and STAT3 and is critical for the regulation of self-renewal in embryonic stem cells (10,11). JMJD1B is a more widely expressed family member and is frequently deleted in myeloid leukemia (12). JMJD1C (also known as TRIP8) is a co-factor of both the androgen and thyroid receptors and has a potential link to autism (13-15). Members of the JMJD1/JHDM2 family have been shown to demethylate mono-methyl and di-methyl histone H3 (Lys9) (3,8).

1. Kubicek, S. et al. (2006) Ernst Schering Res Found Workshop , 1-27.
2. Lin, W. and Dent, S.Y. (2006) Curr Opin Genet Dev 16, 137-42.
3. Klose, R.J. et al. (2006) Nat Rev Genet 7, 715-27.
4. Cachon-Gonzalez, M.B. et al. (1994) Proc Natl Acad Sci USA 91, 7717-21.
5. Ahmad, W. et al. (1998) Science 279, 720-4.
6. Potter, G.B. et al. (2001) Genes Dev 15, 2687-701.
7. Höög, C. et al. (1991) Mol Reprod Dev 30, 173-81.
8. Yamane, K. et al. (2006) Cell 125, 483-95.
9. Okada, Y. et al. (2007) Nature 450, 119-23.
10. Loh, Y.H. et al. (2007) Genes Dev 21, 2545-57.
11. Ko, S.Y. et al. (2006) Cell Struct Funct 31, 53-62.
12. Hu, Z. et al. (2001) Oncogene 20, 6946-54.
13. Lee, J.W. et al. (1995) Mol Endocrinol 9, 243-54.
14. Wolf, S.S. et al. (2007) Arch Biochem Biophys 460, 56-66.
15. Castermans, D. et al. (2007) Eur J Hum Genet 15, 422-31.

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For Research Use Only. Not For Use In Diagnostic Procedures.