In vitro gap-directed translesion DNA synthesis of an abasic site involving human DNA polymerases epsilon, lambda, and beta
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F11%3A00372429" target="_blank" >RIV/68378050:_____/11:00372429 - isvavai.cz</a>
Výsledek na webu
<a href="http://dx.doi.org/10.1074/jbc.M111.246611" target="_blank" >http://dx.doi.org/10.1074/jbc.M111.246611</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1074/jbc.M111.246611" target="_blank" >10.1074/jbc.M111.246611</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
In vitro gap-directed translesion DNA synthesis of an abasic site involving human DNA polymerases epsilon, lambda, and beta
Popis výsledku v původním jazyce
DNA polymerase (pol) ? is thought to be the leading strand replicase in eukaryotes, whereas pols ? and ? are believed to be mainly involved in re-synthesis steps of DNA repair. DNA elongation by the human pol ? is halted by an abasic site (apurinic/apyrimidinic (AP) site). In this study, we present in vitro evidence that human pols ?, ?, and ? can perform translesion synthesis (TLS) of an AP site in the presence of pol ?, likely by initiating the 3OHs created at the lesion by the arrested pol ?. However, in the case of pols ? and ?, this TLS requires the presence of a DNA gap downstream from the product synthesized by the pol ?, and the optimal gap for efficient TLS is different for the two polymerases. Collectively, our in vitro results support the existence of a mechanism of gap-directed TLS at an AP site involving a switch between the replicative pol ? and the repair pols ? and ?.
Název v anglickém jazyce
In vitro gap-directed translesion DNA synthesis of an abasic site involving human DNA polymerases epsilon, lambda, and beta
Popis výsledku anglicky
DNA polymerase (pol) ? is thought to be the leading strand replicase in eukaryotes, whereas pols ? and ? are believed to be mainly involved in re-synthesis steps of DNA repair. DNA elongation by the human pol ? is halted by an abasic site (apurinic/apyrimidinic (AP) site). In this study, we present in vitro evidence that human pols ?, ?, and ? can perform translesion synthesis (TLS) of an AP site in the presence of pol ?, likely by initiating the 3OHs created at the lesion by the arrested pol ?. However, in the case of pols ? and ?, this TLS requires the presence of a DNA gap downstream from the product synthesized by the pol ?, and the optimal gap for efficient TLS is different for the two polymerases. Collectively, our in vitro results support the existence of a mechanism of gap-directed TLS at an AP site involving a switch between the replicative pol ? and the repair pols ? and ?.
Klasifikace
Druh
J<sub>x</sub> - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)
CEP obor
EB - Genetika a molekulární biologie
OECD FORD obor
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Návaznosti výsledku
Projekt
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Návaznosti
Z - Vyzkumny zamer (s odkazem do CEZ)
Ostatní
Rok uplatnění
2011
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Journal of Biological Chemistry
ISSN
0021-9258
e-ISSN
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Svazek periodika
286
Číslo periodika v rámci svazku
37
Stát vydavatele periodika
US - Spojené státy americké
Počet stran výsledku
11
Strana od-do
32094-32104
Kód UT WoS článku
000294726800019
EID výsledku v databázi Scopus
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