FBH1 Helicase Disrupts RAD51 Filaments in Vitro and Modulates Homologous Recombination in Mammalian Cells

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F13%3A00423311" target="_blank" >RIV/68378050:_____/13:00423311 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1074/jbc.M113.484493" target="_blank" >http://dx.doi.org/10.1074/jbc.M113.484493</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1074/jbc.M113.484493" target="_blank" >10.1074/jbc.M113.484493</a>

Jazyk výsledku

angličtina

Název v původním jazyce

FBH1 Helicase Disrupts RAD51 Filaments in Vitro and Modulates Homologous Recombination in Mammalian Cells

Popis výsledku v původním jazyce

Background: Homologous recombination is regulated both positively and negatively in eukaryotic cells to suppress genomic instability. Results: FBH1 can disrupt RAD51 filaments in vitro and suppresses formation of spontaneous RAD51 foci in mammalian cells. In cells defective for FBH1, hyper-recombination is observed. Conclusion: FBH1 is a negative regulator of homologous recombination. Significance: RAD51 activity must be carefully controlled to preserve genomic integrity. Efficient repair of DNA doublestrand breaks and interstrand cross-links requires the homologous recombination (HR) pathway, a potentially error-free process that utilizes a homologous sequence as a repair template. A key player in HR is RAD51, the eukaryotic ortholog of bacterial RecA protein. RAD51 can polymerize on DNA to form a nucleoprotein filament that facilitates both the search for the homologous DNA sequences and the subsequent DNA strand invasion required to initiate HR. Because of its pivotal role in HR, R

Název v anglickém jazyce

FBH1 Helicase Disrupts RAD51 Filaments in Vitro and Modulates Homologous Recombination in Mammalian Cells

Popis výsledku anglicky

Background: Homologous recombination is regulated both positively and negatively in eukaryotic cells to suppress genomic instability. Results: FBH1 can disrupt RAD51 filaments in vitro and suppresses formation of spontaneous RAD51 foci in mammalian cells. In cells defective for FBH1, hyper-recombination is observed. Conclusion: FBH1 is a negative regulator of homologous recombination. Significance: RAD51 activity must be carefully controlled to preserve genomic integrity. Efficient repair of DNA doublestrand breaks and interstrand cross-links requires the homologous recombination (HR) pathway, a potentially error-free process that utilizes a homologous sequence as a repair template. A key player in HR is RAD51, the eukaryotic ortholog of bacterial RecA protein. RAD51 can polymerize on DNA to form a nucleoprotein filament that facilitates both the search for the homologous DNA sequences and the subsequent DNA strand invasion required to initiate HR. Because of its pivotal role in HR, R

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

<a href="/cs/project/GAP305%2F10%2F0281" target="_blank" >GAP305/10/0281: Role of the Rothmund-Thomson syndrome gene product in maintenance of genomic stability</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Journal of Biological Chemistry

ISSN

0021-9258

e-ISSN

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Svazek periodika

288

Číslo periodika v rámci svazku

47

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

34168-34180

Kód UT WoS článku

000327250200060

EID výsledku v databázi Scopus

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