| Literature DB >> 21458466 |
Tae Moon Kim1, Jun Ho Ko, Yong Jun Choi, Lingchuan Hu, Paul Hasty.
Abstract
Fanconi anemia (FA) is a rare autosomal recessive disease characterized by bone marrow failure, developmental defects and cancer. There are multiple FA genes that enable the repair of interstrand crosslinks (ICLs) in coordination with a variety of other DNA repair pathways in a way that is poorly understood. Here we present the phenotype of mouse embryonic stem (ES) cells mutated for FancB. We found FancB-mutant cells exhibited reduced cellular proliferation, hypersensitivity to the crosslinking agent mitomycin C (MMC), increased spontaneous and MMC-induced chromosomal abnormalities, reduced spontaneous sister chromatid exchanges (SCEs), reduced gene targeting, reduced MMC-induced Rad51 foci and absent MMC-induced FancD2 foci. Since FancB is on the X chromosome and since ES cells are typically XY, FancB is an excellent target for an epistatic analysis to elucidate FA's role in ICL repair. Published by Elsevier B.V.Entities:
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Year: 2011 PMID： 21458466 PMCID： PMC3109163 DOI： 10.1016/j.mrfmmm.2011.03.010
Source DB: PubMed Journal: Mutat Res ISSN： 0027-5107 Impact factor: 2.433