Regulation and roles of Cdc7 kinase under replication stress

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F14%3A33149709" target="_blank" >RIV/61989592:15110/14:33149709 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.4161/cc.29251" target="_blank" >http://dx.doi.org/10.4161/cc.29251</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4161/cc.29251" target="_blank" >10.4161/cc.29251</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Regulation and roles of Cdc7 kinase under replication stress

Popis výsledku v původním jazyce

Cdc7 (cell division cycle 7) kinase together with its activation subunit ASK (also known as Dbf4) play pivotal roles in DNA replication and contribute also to other aspects of DNA metabolism such as DNA repair and recombination. While the biological significance of Cdc7 is widely appreciated, the molecular mechanisms through which Cdc7 kinase regulates these various DNA transactions remain largely obscure, including the role of Cdc7-ASK/ Dbf4 under replication stress, a condition associated with diverse(patho) physiological scenarios. In this review, we first highlight the recent findings on a novel pathway that regulates the stability of the human Cdc7-ASK/ Dbf4 complex under replication stress, its interplay with ATR-Chk1 signaling, and significancein the RAD18-dependent DNA damage bypass pathway. We also consider Cdc7 function in a broader context, considering both physiological conditions and pathologies associated with enhanced replication stress, particularly oncogenic transfor

Název v anglickém jazyce

Regulation and roles of Cdc7 kinase under replication stress

Popis výsledku anglicky

Cdc7 (cell division cycle 7) kinase together with its activation subunit ASK (also known as Dbf4) play pivotal roles in DNA replication and contribute also to other aspects of DNA metabolism such as DNA repair and recombination. While the biological significance of Cdc7 is widely appreciated, the molecular mechanisms through which Cdc7 kinase regulates these various DNA transactions remain largely obscure, including the role of Cdc7-ASK/ Dbf4 under replication stress, a condition associated with diverse(patho) physiological scenarios. In this review, we first highlight the recent findings on a novel pathway that regulates the stability of the human Cdc7-ASK/ Dbf4 complex under replication stress, its interplay with ATR-Chk1 signaling, and significancein the RAD18-dependent DNA damage bypass pathway. We also consider Cdc7 function in a broader context, considering both physiological conditions and pathologies associated with enhanced replication stress, particularly oncogenic transfor

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

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2014

Kód důvěrnosti údajů

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

Název periodika

Cell cycle

ISSN

1538-4101

e-ISSN

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Svazek periodika

13

Číslo periodika v rámci svazku

12

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

1859-1866

Kód UT WoS článku

000337944100009

EID výsledku v databázi Scopus

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