Product Pathways - Chromatin Regulation / Epigenetics
JARID1A (D28B10) Rabbit mAb #3876
|3876S||100 µl (10 western blots)||---||In Stock||---|
|3876P||40 µl (4 western blots)||---||In Stock||---|
|3876||carrier free and custom formulation / quantity||email request|
|W||1:1000||Human, Mouse||Endogenous||200||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation
Species predicted to react based on 100% sequence homology: Rat, Bovine.
Specificity / Sensitivity
JARID1A (D28B10) Rabbit mAb detects endogenous levels of total JARID1A protein (both isoforms). The antibody does not cross-react with other JARID proteins, including JARID1B, JARID1C and JARID1D.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the human JARID1A protein.
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.
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