Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

BRCA1 (D54A8) Rabbit mAb #9025

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H Endogenous 220 Rabbit IgG

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

Protocols

Specificity / Sensitivity

BRCA1 (D54A8) Rabbit mAb recognizes endogenous levels of total BRCA1 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a recombinant protein specific to the amino terminus of human BRCA1 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines using BRCA1 (D54A8) Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from MCF7 cells, deprived of serum for 24 hr and either untreated (-) or serum-treated for 18 hr (+), using BRCA1 (D54A8) Rabbit mAb.

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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