Reports summarize cell biology research from National Institute of Immunology
2007 AUG 27 -- A report, "BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination," is newly published data in The Journal of Cell Biology. According to recent research from New Delhi, India, "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," wrote V. Tripathi and colleagues, National Institute of Immunology. The researchers concluded: "These results provide evidence regarding the cooperation between BLM and 53BP1 during maintenance of genomic integrity." Tripathi and colleagues published their study in the Journal of Cell Biology (BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination. Journal of Cell Biology, 2007;178(1):9-14). For additional information, contact V. Tripathi, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi 110067, India. Publisher contact information for the Journal of Cell Biology is: Rockefeller University Press, 1114 First Avenue, 4TH FL, New York, NY 10021, USA. Keywords: India, New Delhi, Cell Biology, Enzyme Research, Genetics, Helicase. This article was prepared by Proteomics Weekly editors from staff and other reports. Copyright 2007, Proteomics Weekly via NewsRx.com.
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