Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14310%2F13%3A00076506" target="_blank" >RIV/00216224:14310/13:00076506 - isvavai.cz</a>

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication

Popis výsledku v původním jazyce

Complex networks of redundant surveillance mechanisms, namely evolutionarily conserved DNA damage response (DDR) and checkpoints, maintain genomic integrity following various genomic insults. Exploring synthetic lethal interactions between DNA repair pathways have wide appliance to the treatment of many types of malignancies. One of the key players in genome surveillance pathways is a protein kinase, CHK1. DNA damage and replication stress supposedly induces activation of CHK1, which then transduces thecheckpoint signal and aids cell cycle arrest allowing time for DNA repair. Hence, CHK1 represents druggable molecular target for inhibition following replication stress induced by chemotherapeutic agents. Such synthetic lethal interaction leads to enhanced sensitivity of cancer cells with additional burden of damaged DNA, without cytotoxic effects to the normal cells.

Název v anglickém jazyce

Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication

Popis výsledku anglicky

Complex networks of redundant surveillance mechanisms, namely evolutionarily conserved DNA damage response (DDR) and checkpoints, maintain genomic integrity following various genomic insults. Exploring synthetic lethal interactions between DNA repair pathways have wide appliance to the treatment of many types of malignancies. One of the key players in genome surveillance pathways is a protein kinase, CHK1. DNA damage and replication stress supposedly induces activation of CHK1, which then transduces thecheckpoint signal and aids cell cycle arrest allowing time for DNA repair. Hence, CHK1 represents druggable molecular target for inhibition following replication stress induced by chemotherapeutic agents. Such synthetic lethal interaction leads to enhanced sensitivity of cancer cells with additional burden of damaged DNA, without cytotoxic effects to the normal cells.

Druh

O - Ostatní výsledky

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

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Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2013

Kód důvěrnosti údajů

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