53BP1 Regulates DSB Repair Using Rif1 to Control 5 ' End Resection

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F13%3A00066922" target="_blank" >RIV/00216224:14740/13:00066922 - isvavai.cz</a>
Result on the web
<a href="http://dx.doi.org/10.1126/science.1231573" target="_blank" >http://dx.doi.org/10.1126/science.1231573</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1126/science.1231573" target="_blank" >10.1126/science.1231573</a>

Result language
angličtina
Original language name
53BP1 Regulates DSB Repair Using Rif1 to Control 5 ' End Resection
Original language description
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 controlof DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.
Czech name
—
Czech description
—

Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
EB - Genetics and molecular biology
OECD FORD branch
—

Project
<a href="/en/project/GAP205%2F12%2F0550" target="_blank" >GAP205/12/0550: Dynamics of shelterin complex assembly</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Publication year
2013
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Similar results(10)