PFM01 is a cell-permeable N-alkylated Mirin (Sigma Cat. No. 475954) derivative that selectively inhibits against MRE11 endo-, but not exo-, nuclease activity. PFM01 targets MRE11 at a site near the dimer interface, distinct from that occupied by Mirin and PFM39 to allow disruption of the ssDNA-binding groove and selective inhibition against MRE11 endo-, but not exo-, nuclease activity. While both endonuclease and exonuclease activities are required for MRE11-mediated homologous recombination (HR) repair, only FM01 (100 μM), but not the exonuclease inhibitors Mirin (500 μM) and PFM39 (100 μM), rescues G2-phase double-strand break (DSB) repair defect in HR protein BRCA2-deficient HSC62-hTERT fibroblasts following ionizing irradiation (IR) by blocking HR initiation and thereby allowing non-homologous end joining (NHEJ) to proceed.
Cell chemical biology, 24(9), 1101-1119 (2017-09-25)
To maintain stable genomes and to avoid cancer and aging, cells need to repair a multitude of deleterious DNA lesions, which arise constantly in every cell. Processes that support genome integrity in normal cells, however, allow cancer cells to develop
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 34(2), 2812-2820 (2020-01-08)
The Mre11A/RAD50/NBN complex (MRN) is an essential regulator of the cellular damage response after DNA double-strand breaks (DSBs). More recent work has indicated that MRN may also impact on the duration of mitosis. We show here that RAD50-deficient fibroblasts exhibit
Proceedings of the National Academy of Sciences of the United States of America, 118(11) (2021-03-13)
Homologous recombination (HR) is a major pathway for repair of DNA double-strand breaks (DSBs). The initial step that drives the HR process is resection of DNA at the DSB, during which a multitude of nucleases, mediators, and signaling proteins accumulates
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