Cell Signaling Technology

Product Pathways - Chromatin Regulation / Epigenetics

JARID1C (D29B9) Rabbit mAb #5361

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M (Mk) (Pg) (Hr) Endogenous 180 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  Mk=Monkey  Pg=Pig  Hr=Horse
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

JARID1C (D29B9) Rabbit mAb detects endogenous levels of total JARID1C protein. The antibody does not cross-react with other JARID proteins, including JARID1A, JARID1B and JARID1D.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu830 of human JARID1C protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from NCCIT and F9 cell lines using JARID1C (D29B9) Rabbit mAb.

Background

The methylation state of lysine residues in histone proteins is a major determinant for formation of active and inactive regions of the genome and is crucial for 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 can 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 7 separate families (3). The JARID (Jumonji/AT-rich interactive domain-containing protein) family contains four members: JARID1A (also RBP2 and RBBP2), JARID1B (also PLU-1), JARID1C (also SMCX) and JARID1D (also SMCY) (4). In addition to the JmJC domain, these proteins contain JmJN, BRIGHT, C5HC2 zinc-finger, and PHD domains, the latter of which binds to methylated histone H3 (Lys9) (4). All four JARID proteins demethylate di- and tri-methyl histone H3 Lys4; JARID1B also demethylates mono-methyl histone H3 Lys4 (5-7). JARID1A is a critical RB-interacting protein and is required for Polycomb-Repressive Complex 2 (PRC2)-mediated transcriptional repression during ES cell differentiation (8). A JARID1A-NUP98 gene fusion is associated with myeloid leukemia (9). JARID1B, which interacts with many proteins including c-Myc and HDAC4, may play a role in cell fate decisions by blocking terminal differentiation (10-12). JARID1B is over-expressed in many breast cancers and may act by repressing multiple tumor suppressor genes including BRCA1 and HOXA5 (13,14). JARID1C has been found in a complex with HDAC1, HDAC2, G9a and REST, which binds to and represses REST target genes in non-neuronal cells (7). JARID1C mutations are associated with X-linked mental retardation and epilepsy (15,16). JARID1D is largely uncharacterized.

  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. Benevolenskaya, E.V. (2007) Biochem Cell Biol 85, 435-43.
  5. Christensen, J. et al. (2007) Cell 128, 1063-76.
  6. Yamane, K. et al. (2007) Mol Cell 25, 801-12.
  7. Tahiliani, M. et al. (2007) Nature 447, 601-5.
  8. Pasini, D. et al. (2008) Genes Dev 22, 1345-55.
  9. van Zutven, L.J. et al. (2006) Genes Chromosomes Cancer 45, 437-46.
  10. Secombe, J. et al. (2007) Genes Dev 21, 537-51.
  11. Barrett, A. et al. (2007) Int J Cancer 121, 265-75.
  12. Dey, B.K. et al. (2008) Mol Cell Biol 28, 5312-27.
  13. Barrett, A. et al. (2002) Int J Cancer 101, 581-8.
  14. Lu, P.J. et al. (1999) J Biol Chem 274, 15633-45.
  15. Tzschach, A. et al. (2006) Hum Mutat 27, 389.
  16. Jensen, L.R. et al. (2005) Am J Hum Genet 76, 227-36.

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