Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

BRCA1 (A8X9F) Rabbit mAb #14823

No. Size Price
14823S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
14823 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human, Endogenous 220 Rabbit IgG
IP 1:50

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting, IP=Immunoprecipitation,

Specificity / Sensitivity

BRCA1 (A8X9F) 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 HT-29, HeLa, and MCF7 cells using BRCA1 (A8X9F) 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, 1021-9.
  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.

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

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