Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

Phospho-BACH1/BRIP1 (Thr1133) Antibody #11983

Applications Reactivity Sensitivity MW (kDa) Source
W IP H Mk Endogenous 145 Rabbit

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

Protocols

Specificity / Sensitivity

Phospho-BACH1/BRIP1 (Thr1133) Antibody recognizes endogenous levels of BACH1/BRIP1 protein only when phosphorylated at Thr1133. This antibody also cross-reacts with a protein of unknown origin at ~130 kDa.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Thr1133 of human BACH1/BRIP1 protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from Jurkat cells, untreated (-) or treated with λ phosphatase and calf intestinal phosphatase (CIP) (+), using Phospho-BACH1/BRIP1 (Thr1133) Antibody (upper) or BACH1/BRIP1 Antibody #4578 (lower).

IP

IP

Immunoprecipitation of phospho-BACH1/BRIP1 (Thr1133) from 293T cell extracts using Normal Rabbit IgG #2729 (lane 2) or Phospho-BACH1/BRIP1 (Thr1133) Antibody (lane 3). Lane 1 is 10% input. Western blot analysis was performed using Phospho-BACH1/BRIP1 (Thr1133) Antibody.

Background

BACH1, also known as BRIP1 and FANCJ, is a DNA helicase involved in repair of DNA cross-links and double strand breaks (1-3). Interaction between phosphorylated BACH1 and BRCA1 is required for DNA damage-induced checkpoint signaling (3,4). Originally identified as a breast cancer susceptibility gene (1), the BACH1 gene is mutated in Fanconi anemia (5), a recessive disorder characterized by multiple congenital abnormalities, progressive bone marrow failure, and high cancer risk/predisposition. Research investigators have concluded that BACH1 interactions with BRCA1 and the presence of BACH1 mutations in patients with early onset breast cancer indicate that BACH1 may act as a tumor suppressor (6).Phosphorylation of BACH1 at Thr1133 is thought to be involved in regulation of the replication checkpoint and is required for the interaction of BACH1 with TopBP1 (7).

  1. Cantor, S.B. et al. (2001) Cell 105, 149-60.
  2. Litman, R. et al. (2005) Cancer Cell 8, 255-65.
  3. Peng, M. et al. (2006) Oncogene 25, 2245-53.
  4. Shiozaki, E.N. et al. (2004) Mol Cell 14, 405-12.
  5. Kennedy, R.D. and D'Andrea, A.D. (2005) Genes Dev 19, 2925-40.
  6. Cantor, S.B. and Guillemette, S. (2011) Future Oncol 7, 253-61.
  7. Gong, Z. et al. (2010) Mol Cell 37, 438-46.

Application References

Have you published research involving the use of our products? If so we'd love to hear about it. Please let us know!

Companion Products

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

Products