53BP1: pro choice in DNA repair

نویسندگان
چکیده

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

53BP1: pro choice in DNA repair.

The DNA damage response factor 53BP1 functions at the intersection of two major double strand break (DSB) repair pathways--promoting nonhomologous end-joining (NHEJ) and inhibiting homology-directed repair (HDR)--and integrates cellular inputs to ensure their timely execution in the proper cellular contexts. Recent work has revealed that 53BP1 controls 5' end resection at DNA ends, mediates syn...

متن کامل

DNA repair pathway choice--a PTIP of the hat to 53BP1.

hot off the press hot off the press D NA double-stranded breaks (DSBs) are highly cytotoxic lesions that can induce genome rearrangements if not accurately repaired. DSBs can be repaired either through homologous recombination (HR) or non-homologous end-joining (NHEJ). HR is the preferred repair pathway during the S and G2 cell cycle phases because a sister chromatid provides a perfect template...

متن کامل

PARP2 controls double-strand break repair pathway choice by limiting 53BP1 accumulation at DNA damage sites and promoting end-resection

Double strand breaks (DSBs) are one of the most toxic lesions to cells. DSB repair by the canonical non-homologous end-joining (C-EJ) pathway involves minor, if any, processing of the broken DNA-ends, whereas the initiation of DNA resection channels the broken-ends toward DNA repair pathways using various lengths of homology. Mechanisms that control the resection initiation are thus central to ...

متن کامل

BRCA1-associated exclusion of 53BP1 from DNA damage sites underlies temporal control of DNA repair.

Following irradiation, numerous DNA-damage-responsive proteins rapidly redistribute into microscopically visible subnuclear aggregates, termed ionising-radiation-induced foci (IRIF). How the enrichment of proteins on damaged chromatin actually relates to DNA repair remains unclear. Here, we use super-resolution microscopy to examine the spatial distribution of BRCA1 and 53BP1 proteins within si...

متن کامل

MOF phosphorylation by ATM regulates 53BP1-mediated double-strand break repair pathway choice.

Cell-cycle phase is a critical determinant of the choice between DNA damage repair by nonhomologous end-joining (NHEJ) or homologous recombination (HR). Here, we report that double-strand breaks (DSBs) induce ATM-dependent MOF (a histone H4 acetyl-transferase) phosphorylation (p-T392-MOF) and that phosphorylated MOF colocalizes with γ-H2AX, ATM, and 53BP1 foci. Mutation of the phosphorylation s...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Trends in Cell Biology

سال: 2014

ISSN: 0962-8924

DOI: 10.1016/j.tcb.2013.09.003