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• W2054678629 startingPage "26349" @default.
• W2054678629 abstract "Loss or inactivation of BLM, a helicase of the RecQ family, causes Bloom syndrome, a genetic disorder with a strong predisposition to cancer. Although the precise function of BLM remains unknown, genetic data has implicated BLM in the process of genetic recombination and DNA repair. Previously, we demonstrated that BLM can disrupt the RAD51-single-stranded DNA filament that promotes the initial steps of homologous recombination. However, this disruption occurs only if RAD51 is present in an inactive ADP-bound form. Here, we investigate interactions of BLM with the active ATP-bound form of the RAD51-single-stranded DNA filament. Surprisingly, we found that BLM stimulates DNA strand exchange activity of RAD51. In contrast to the helicase activity of BLM, this stimulation does not require ATP hydrolysis. These data suggest a novel BLM function that is stimulation of the RAD51 DNA pairing. Our results demonstrate the important role of the RAD51 nucleoprotein filament conformation in stimulation of DNA pairing by BLM." @default.
• W2054678629 created "2016-06-24" @default.
• W2054678629 creator A5023103944 @default.
• W2054678629 creator A5048980451 @default.
• W2054678629 creator A5071817184 @default.
• W2054678629 date "2009-09-01" @default.
• W2054678629 modified "2023-09-30" @default.
• W2054678629 title "Bloom Syndrome Helicase Stimulates RAD51 DNA Strand Exchange Activity through a Novel Mechanism" @default.
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• W2054678629 doi "https://doi.org/10.1074/jbc.m109.029371" @default.
• W2054678629 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2786030" @default.
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• W2054678629 hasPublicationYear "2009" @default.
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