KREJČÍ, Lumír. DNA repair mechanisms in yeast. In 37th Annual Conference on Yeast. 37th Annual Conference o. Bratislava, Slovakia: Visegrad Strategic Program. 113 s. ISSN 1336-4839. 2009.
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Základní údaje
Originální název DNA repair mechanisms in yeast
Název česky DNA opravné mechanismy u kvasinek
Autoři KREJČÍ, Lumír.
Vydání 37th Annual Conference o. Bratislava, Slovakia, 37th Annual Conference on Yeast, 113 s. 2009.
Nakladatel Visegrad Strategic Program
Další údaje
Originální jazyk angličtina
Typ výsledku Stať ve sborníku
Obor 10600 1.6 Biological sciences
Stát vydavatele Slovensko
Utajení není předmětem státního či obchodního tajemství
WWW URL
Organizační jednotka Lékařská fakulta
ISSN 1336-4839
Klíčová slova anglicky DNA repair; DNA damage; replication; genomic instability
Štítky DNA damage, DNA repair, genomic instability, replication
Příznaky Mezinárodní význam
Změnil Změnil: doc. Mgr. Lumír Krejčí, Ph.D., učo 18098. Změněno: 23. 4. 2010 15:30.
Anotace
DNA replication is typically highly processive mechanism with astonishing precision, despite the fact that it frequently encounters barriers caused by endogenous and exogenous genotoxic agents. It is not surprising that DNA replication does not act alone, but operates in coordination with homologous recombination (HR), and other DNA repair processes to overcome such replication obstacles to ensure cellular viability, and achieve genomic stability. Numerous mechanisms by which replication forks can be restarted following arrest have been described. Some of the pathways enable the cells to deal with such impediments while keeping the fork in place, including repriming, template switch, and translesion synthesis, others may provoke partial or complete fork collapse followed by fork reversal. This could not only provide time and space for repair but also liberate the new strand to undergo template switch. Alternatively, the fork can be cleaved, creating the DSB break that is repaired by recombination machinery with ability to restart the replication fork. Inability to remove toxic DNA structures often leads to their accumulation, higher mutation frequency and eventually to cancer or other diseases associated with genomic instability.
Anotace česky
DNA replication is typically highly processive mechanism with astonishing precision, despite the fact that it frequently encounters barriers caused by endogenous and exogenous genotoxic agents. It is not surprising that DNA replication does not act alone, but operates in coordination with homologous recombination (HR), and other DNA repair processes to overcome such replication obstacles to ensure cellular viability, and achieve genomic stability. Numerous mechanisms by which replication forks can be restarted following arrest have been described. Some of the pathways enable the cells to deal with such impediments while keeping the fork in place, including repriming, template switch, and translesion synthesis, others may provoke partial or complete fork collapse followed by fork reversal. This could not only provide time and space for repair but also liberate the new strand to undergo template switch. Alternatively, the fork can be cleaved, creating the DSB break that is repaired by recombination machinery with ability to restart the replication fork. Inability to remove toxic DNA structures often leads to their accumulation, higher mutation frequency and eventually to cancer or other diseases associated with genomic instability.
Návaznosti
GA301/09/1917, projekt VaVNázev: Štěpení replikačních-rekombinačních DNA meziproduktů a jejich úloha při nestabilitě genomu
Investor: Grantová agentura ČR, Štěpení replikačních-rekombinačních DNA meziproduktů a jejich úloha při nestabilitě genomu
GD203/09/H046, projekt VaVNázev: Biochemie na rozcestí mezi in silico a in vitro
Investor: Grantová agentura ČR, Biochemie na rozcestí mezi in silico a in vitro
LC06030, projekt VaVNázev: Biomolekulární centrum
Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Biomolekulární centrum
MSM0021622413, záměrNázev: Proteiny v metabolismu a při interakci organismů s prostředím
Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Proteiny v metabolismu a při interakci organismů s prostředím
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