Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication
The result's identifiers
Result code in 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>
Result on the web
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DOI - Digital Object Identifier
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Alternative languages
Result language
angličtina
Original language name
Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication
Original language description
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.
Czech name
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Czech description
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Classification
Type
O - Miscellaneous
CEP classification
CE - Biochemistry
OECD FORD branch
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Result continuities
Project
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Continuities
S - Specificky vyzkum na vysokych skolach
Others
Publication year
2013
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů