Cell Signaling Technology

Product Pathways - DNA Damage

BRCA2 Antibody #9012

Applications Reactivity Sensitivity MW (kDa) Source
W H M B Endogenous 380 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  B=Bovine
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

BRCA2 Antibody detects endogenous levels of total BRCA2 protein. The antibody does not recognize BRCA1.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acids near the amino terminus of human BRCA2. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from human (HeLa), murine (SV-T2) and bovine (BAEC) cells using BRCA2 Antibody.

Background

The breast cancer susceptibility proteins BRCA1 and BRCA2 are frequently mutated in cases of hereditary breast and ovarian cancers and have roles in multiple processes related to DNA damage, repair, cell cycle progression, transcription, ubiquitination, and apoptosis (1-4). BRCA2 has been shown to be required for localization of Rad51 to sites of double stranded breaks (DSBs) in DNA, and cells lacking BRCA1 and BRCA2 cannot repair DSBs through the Rad51-dependent process of homologous recombination (HR) (5). Numerous DNA damage-induced phosphorylation sites on BRCA1 have been identified, including Ser988, 1189, 1387, 1423, 1457, 1524 and 1542, and kinases activated in a cell cycle-dependent manner, including Aurora A and CDK2, can also phosphorylate BRCA1 at Ser308 and Ser1497, respectively (6-10). Cell cycle-dependent phosphorylation of BRCA2 at Ser3291 by CDKs has been proposed as a mechanism to switch off HR as cells progress beyond S-phase by blocking the carboxy terminal Rad51 binding site (11).

  1. Rahman, N. and Stratton, M.R. (1998) Annu. Rev. Genet. 32, 95-121.
  2. Gayther, S. A. et al. (1999) Am. J. Hum. Genet. 65, 1021-1029.
  3. Kerr, P. and Ashworth, A. (2001) Curr. Biol. 11, R668-R676.
  4. Scully, R. and Livingston, D.M. (2000) Nature 408, 429-432.
  5. Tutt, A. and Ashworth, A. (2002) Trends Mol. Med. 8, 571-576.
  6. Okada, S. and Ouchi, T. (2003) J. Biol. Chem. 278, 2015-2020.
  7. Cortez, D. et al. (1999) Science 286, 1162-1166.
  8. Xu, B. et al. (2002) Cancer Res. 62, 4588-4591.
  9. Ouchi, M. et al. (2004) J. Biol. Chem. 279, 19643-19648.
  10. Ruffner, H. et al. (1999) Mol. Cell. Biol. 19, 4843-4854.
  11. Esashi, F. et al. (2005) Nature 434, 598-604.

Application References

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Companion Products

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

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