SAMADDER, Pounami. Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication. In Central European DNA Repair Meeting. 2013.
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Základní údaje
Originální název Exploring synthetic lethal interaction between Checkpoint Kinase 1(CHK1) and DNA replication
Autoři SAMADDER, Pounami (356 Indie, garant, domácí).
Vydání Central European DNA Repair Meeting, 2013.
Další údaje
Originální jazyk angličtina
Typ výsledku Prezentace na konferencích
Obor 10600 1.6 Biological sciences
Stát vydavatele Česká republika
Utajení není předmětem státního či obchodního tajemství
WWW URL
Kód RIV RIV/00216224:14310/13:00076506
Organizační jednotka Přírodovědecká fakulta
Klíčová slova anglicky CHK1 DNA repair cancer
Změnil Změnila: Pounami Samadder, Ph.D., učo 404286. Změněno: 21. 9. 2014 10:39.
Anotace
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 the checkpoint 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.
Anotace česky
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 the checkpoint 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.
VytisknoutZobrazeno: 8. 5. 2024 04:06