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Phosphorylation-dependent interactions of BLM and 53BP1 are required for their anti-recombinogenic roles during homologous recombination

Mutations in bloom helicase protein (BLM) helicase cause Bloom syndrome, characterized by predisposition to almost all forms of cancer. We have demonstrated previously that endogenous BLM, signal transducer 53BP1 and RAD51 are present in a complex during replication stress. Using full-length recombi...

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Main Authors: Tripathi, Vivek, Kaur, Sarabpreet, Sengupta, Sagar
Formato: Artigo
Idioma:Inglês
Publicado: 2007
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Acceso en liña:https://ncbi.nlm.nih.gov/pmc/articles/PMC2365705/
https://ncbi.nlm.nih.gov/pubmed/17984114
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1093/carcin/bgm238
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