GSBS Student Publications
Title
BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ
Publication Date
2005-09-13
UMMS Affiliation
Graduate School of Biomedical Sciences; Department of Cancer Biology; Program in Molecular Medicine
Document Type
Article
Disciplines
Life Sciences | Medicine and Health Sciences
Abstract
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.
DOI of Published Version
10.1016/j.ccr.2005.08.004
Source
Cancer Cell. 2005 Sep;8(3):255-65. Link to article on publisher's site
Journal/Book/Conference Title
Cancer cell
Related Resources
PubMed ID
16153896
Repository Citation
Litman, Rachel; Peng, Min; Jin, Zhe; Zhang, Fan; Zhang, Junran; Powell, Simon N.; Andreassen, Paul R.; and Cantor, Sharon B., "BACH1 is critical for homologous recombination and appears to be the Fanconi anemia gene product FANCJ" (2005). GSBS Student Publications. 771.
https://escholarship.umassmed.edu/gsbs_sp/771