BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ
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Authors
Litman, RachelPeng, Min
Jin, Zhe
Zhang, Fan
Zhang, Junran
Powell, Simon N.
Andreassen, Paul R.
Cantor, Sharon B.
UMass Chan Affiliations
Program in Molecular MedicineDepartment of Cancer Biology
Graduate School of Biomedical Sciences
Document Type
Journal ArticlePublication Date
2005-09-13Keywords
Basic-Leucine Zipper Transcription Factors; Breast Neoplasms; Cell Division; Cell Line, Tumor; Chromosome Mapping; DNA Primers; Fanconi Anemia; Fanconi Anemia Complementation Group Proteins; Female; G2 Phase; Genes, Reporter; Green Fluorescent Proteins; Humans; Leucine Zippers; *Recombination, Genetic; Transcription Factors; TransfectionLife Sciences
Medicine and Health Sciences
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Show full item recordAbstract
We showed in this study that cells deficient of the BRCA1-associated BACH1 helicase, also known as BRIP1, failed to elicit homologous recombination (HR) after DNA double-stranded breaks (DSBs). BACH1-deficient cells were also sensitive to mitomycin C (MMC) and underwent MMC-induced chromosome instability. Moreover, we identified a homozygous nonsense mutation in BACH1 in a FA-J patient-derived cell line and could not detect BACH1 protein in this cell line. Expression of wild-type BACH1 in this cell line reduced the accumulation of cells at G2/M phases following exposure to DNA crosslinkers, a characteristic of Fanconi anemia (FA) cells. These results support the conclusion that BACH1 is FANCJ.Source
Cancer Cell. 2005 Sep;8(3):255-65. Link to article on publisher's siteDOI
10.1016/j.ccr.2005.08.004Permanent Link to this Item
http://hdl.handle.net/20.500.14038/34107PubMed ID
16153896Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.ccr.2005.08.004