New England Biolabs Canada
 

Product Pathways - DNA Damage

BRCA1 Antibody #9010

Item# Description List Price Web Price Qty
9010S BRCA1 Antibody - 100 µl $364.00
$327.60
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9010T BRCA1 Antibody - 20 µl $155.00
$139.50
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*On-line ordering is for Canadian customers only. Web pricing is applicable only to orders placed online at www.neb.ca
VIEW COMPANION PRODUCTS HIDE COMPANION PRODUCTS
Application Dilution Species-Reactivity Sensitivity MW (kDa) Source
W Human Endogenous 220 Rabbit
IP

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation

Specificity / Sensitivity

BRCA1 Antibody detects endogenous levels of total BRCA1 protein. Five human isoforms are produced by alternative splicing and alternative initiation. The nuclear isoforms 1, 2, and 4 are detected, whereas the cytoplasmic isoforms 3 and 5 are not. The antibody does not recognize BRCA2.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acids near the amino terminus of human BRCA1. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of untreated and UV-treated (50 mJ/cm2, 30 min) HeLa cells, using BRCA1 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, 1021-9.
  3. Kerr, P. and Ashworth, A. (2001) Curr Biol 11, R668-76.
  4. Scully, R. and Livingston, D.M. (2000) Nature 408, 429-32.
  5. Tutt, A. and Ashworth, A. (2002) Trends Mol Med 8, 571-6.
  6. Okada, S. and Ouchi, T. (2003) J Biol Chem 278, 2015-20.
  7. Cortez, D. et al. (1999) Science 286, 1162-6.
  8. Xu, B. et al. (2002) Cancer Res 62, 4588-91.
  9. Ouchi, M. et al. (2004) J Biol Chem 279, 19643-8.
  10. Ruffner, H. et al. (1999) Mol Cell Biol 19, 4843-54.
  11. Esashi, F. et al. (2005) Nature 434, 598-604.

Application References

  • Stordal, B. et al. (2012) PLoS One 7, e40717. Applications: Western Blotting.

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