HIRA (D2A5E) Rabbit mAb #13307
- WB
Supporting Data
| REACTIVITY | H M Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 112 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Species Reactivity:
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu593 of human HIRA protein.
Background
Histone cell cycle regulation defective homolog A (HIRA), also known as TUP1-like enhancer of split protein 1 (TUPLE1), is the mammalian homolog of the yeast HIR1 and HIR2 transcriptional repressor proteins (1). HIRA interacts with UBN1, CABIN, and ASF1A in the cell nucleus to form the evolutionarily conserved HUCA histone chaperone complex that deposits the variant histone H3.3 into chromatin in a DNA-replication independent manner (2). HIRA is required for deposition of histone H3.3 at the transcription start sites of genes, where incorporation of histone H3.3 facilitates nucleosome destabilization and contributes to transcriptional activation (3-5). Histone H3.3 is also linked to gene silencing and is incorporated into regions of the genome thought to be transcriptionally inactive (5-7). While some incorporation of H3.3 into heterochromatin is facilitated by a different histone chaperone complex that contains ATRX and DAXX (ie. telomeric incorporation of H3.3), HIRA is required for incorporation of histone H3.3 and formation of senescence-associated heterochromatin foci (SAHF) during cellular senescence (5-8). HIRA is ubiquitously expressed during mouse embryonic development (9). In the adult mouse, HIRA is expressed at high levels in the kidney, skeletal muscle, and pancreas, but it is expressed at lower levels in the heart, lung, placenta, brain, and liver (9). A missing copy of the HIRA gene on human chromosome region 22q11.2 is a common characteristic of DiGeorge syndrome patients and insufficient production of the HIRA protein may disrupt normal embryonic development (9).
- Lamour, V. et al. (1995) Hum Mol Genet 4, 791-9.
- Rai, T.S. et al. (2011) Mol Cell Biol 31, 4107-18.
- Jin, C. et al. (2009) Nat Genet 41, 941-5.
- Jin, C. and Felsenfeld, G. (2007) Genes Dev 21, 1519-29.
- Goldberg, A.D. et al. (2010) Cell 140, 678-91.
- Wong, L.H. et al. (2010) Genome Res 20, 351-60.
- Wong, L.H. et al. (2009) Genome Res 19, 404-14.
- Zhang, R. et al. (2007) Mol Cell Biol 27, 2343-58.
- Wilming, L.G. et al. (1997) Hum Mol Genet 6, 247-58.
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