Biochemical mechanism of DSB end resection and its regulation

نویسندگان
چکیده

منابع مشابه

End resection at double-strand breaks: mechanism and regulation.

RecA/Rad51 catalyzed pairing of homologous DNA strands, initiated by polymerization of the recombinase on single-stranded DNA (ssDNA), is a universal feature of homologous recombination (HR). Generation of ssDNA from a double-strand break (DSB) requires nucleolytic degradation of the 5'-terminated strands to generate 3'-ssDNA tails, a process referred to as 5'-3' end resection. The RecBCD helic...

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DNA double-strand breaks (DSBs) are highly hazardous for genome integrity, because failure to repair these lesions can lead to genomic instability. DSBs can arise accidentally at unpredictable locations into the genome, but they are also normal intermediates in meiotic recombination. Moreover, the natural ends of linear chromosomes resemble DSBs. Although intrachromosomal DNA breaks are potent ...

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We developed a biochemical kinetics approach to describe the repair of double strand breaks (DSB) produced by low LET radiation by modeling molecular events associated with the mechanisms of non-homologous end-joining (NHEJ). A system of coupled nonlinear ordinary differential equations describes the induction of DSB and activation pathways for major NHEJ components including Ku70/80, DNA-PKcs,...

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53BP1 regulates DSB repair using Rif1 to control 5' end resection.

The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we ident...

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ژورنال

عنوان ژورنال: DNA Repair

سال: 2015

ISSN: 1568-7864

DOI: 10.1016/j.dnarep.2015.04.015