Binding of double-strand breaks in DNA by human Rad52 protein.

Details

Serval ID
serval:BIB_A637B5568971
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Binding of double-strand breaks in DNA by human Rad52 protein.
Journal
Nature
Author(s)
Van Dyck E., Stasiak A.Z., Stasiak A., West S.C.
ISSN
0028-0836[print], 0028-0836[linking]
Publication state
Published
Issued date
09/1999
Volume
398
Number
6729
Pages
728-731
Language
english
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Abstract
Double-strand breaks (DSBs) in DNA are caused by ionizing radiation. These chromosomal breaks can kill the cell unless repaired efficiently, and inefficient or inappropriate repair can lead to mutation, gene translocation and cancer. Two proteins that participate in the repair of DSBs are Rad52 and Ku: in lower eukaryotes such as yeast, DSBs are repaired by Rad52-dependent homologous recombination, whereas vertebrates repair DSBs primarily by Ku-dependent non-homologous end-joining. The contribution of homologous recombination to vertebrate DSB repair, however, is important. Biochemical studies indicate that Ku binds to DNA ends and facilitates end-joining. Here we show that human Rad52, like Ku, binds directly to DSBs, protects them from exonuclease attack and facilitates end-to-end interactions. A model for repair is proposed in which either Ku or Rad52 binds the DSB. Ku directs DSBs into the non-homologous end-joining repair pathway, whereas Rad52 initiates repair by homologous recombination. Ku and Rad52, therefore, direct entry into alternative pathways for the repair of DNA breaks.
Keywords
Antigens, Nuclear, Cell Line, DNA/genetics, DNA Helicases, DNA Repair/genetics, DNA-Binding Proteins/genetics, DNA-Binding Proteins/physiology, Humans, Models, Genetic, Nuclear Proteins/genetics, Recombination, Genetic, Saccharomyces cerevisiae Proteins, Sequence Homology
Pubmed
Web of science
Create date
24/01/2008 10:35
Last modification date
20/08/2019 15:11
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