Mutations in BLM helicase cause Bloom syndrome, characterized by predisposition to all forms of cancer. We demonstrate that BLM, signal transducer 53BP1, and RAD51 interact during stalled replication. Interactions between the three proteins have functional consequences. Lack of 53BP1 decreases the cell survival and enhanced chromosomal aberration after replication arrest. 53BP1 exhibits both BLM-dependent and -independent anti-recombinogenic functions in human and mouse cells. Both BLM and 53BP1 abrogate endogenous RAD51 foci formation and disrupt RAD51 polymerization. Consequently, loss of BLM and 53BP1 synergistically enhances stress-dependent homologous recombination. These results provide evidence regarding the cooperation between BLM and 53BP1 during maintenance of genomic integrity.
BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Publishing Authors By Initials
BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Journal Published:
PUBLICATION TYPE: Research Support, Non-U.S. Gov
Journal: The Journal of cell biology
VOLUME: 178
Page Numbers: 9-14
Journal Abbreviation: J. Cell Biol.
ISSN: 0021-9525
DAY: 25
MONTH: 06
YEAR: 2007
BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Information
Number of References:
LANGUAGE: eng
NlmUniqueID: 375356
BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Keywords Mesh Terms:
KEYWORDS: Transfection
MESH TERMS: genetics
Chemical & Substance for Abstract: BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Information
Substance Name: DNA Helicases
Registry Number: EC 3.6.1.-
Grant and Affiliation Information for BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination.
AFFILIATION: National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India.
Country: United States
AGENCY: United States FIC
GRANT: 1 R01 TW0073202-01A1
ACRONYM: TW
MEDLINETA: J Cell Biol
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ACCESSION NUMBER:
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