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@misc{727357,
author = {Krejčí, Lumír},
address = {Snowmass},
keywords = {recombination; DNA repair; rearrangements; genome},
language = {eng},
location = {Snowmass},
publisher = {FASEB},
title = {Genetic Recombination & Genome Rearrangements},
url = {http://www.faseb.org},
year = {2007}
}
TY - GEN
ID - 727357
AU - Krejčí, Lumír
PY - 2007
TI - Genetic Recombination & Genome Rearrangements
PB - FASEB
CY - Snowmass
KW - recombination
KW - DNA repair
KW - rearrangements
KW - genome
UR - http://www.faseb.org
L2 - http://www.faseb.org
N2 - Homologous recombination (HR) represents an important means for the repair of chromosome breaks induced by exogenous agents (e.g. ionizing radiation) or that arise endogenously (e.g. replication of a damaged DNA template). Furthermore, cells have to rely on homologous recombination to rescue stalled replication forks and hence prevent fork demise. If not processed properly, DSBs can lead to chromosomal aberrations and rearrangements, which then give rise to strong mutator and cancer phenotypes. DNA strand break repair by HR is mediated by genes of the RAD52 epistasis group. Rad52 protein plays central role in this process. Here, we show that Rad52 competes with Srs2 anti-recombinase in mediating Rad51-catalyzed strand exchange reaction through common interaction site on Rad51. The molecular mechanism of Rad52 function in homologous recombination together with the role of postranslational modification (SUMO-ylation) is discussed.
ER -
KREJČÍ, Lumír. \textit{Genetic Recombination \&{} Genome Rearrangements}. Snowmass: FASEB, 2007.
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