TY - JOUR
T1 - Mechanism of homologous recombination
T2 - Mediators and helicases take on regulatory functions
AU - Sung, Patrick
AU - Klein, Hannah
N1 - Funding Information:
We are grateful to M. Sehorn for providing the electron micrographs in Figure 4 and to J. San Filippo and W. Bussen for their help in preparing the figures. We apologize to colleagues whose work could not be cited because of space limitations. The studies in the laboratories of the authors have been supported by research grants from the US National Institutes of Health, the US Department of Defense and the Susan G. Komen Breast Cancer Foundation.
PY - 2006/10/23
Y1 - 2006/10/23
N2 - Homologous recombination (HR) is an important mechanism for the repair of damaged chromosomes, for preventing the demise of damaged replication forks, and for several other aspects of chromosome maintenance. As such, HR is indispensable for genome integrity, but it must be regulated to avoid deleterious events. Mutations in the tumour-suppressor protein BRCA2, which has a mediator function in HR, lead to cancer formation. DNA helicases, such as Bloom's syndrome protein (BLM), regulate HR at several levels, in attenuating unwanted HR events and in determining the outcome of HR. Defects in BLM are also associated with the cancer phenotype. The past several years have witnessed dramatic advances in our understanding of the mechanism and regulation of HR.
AB - Homologous recombination (HR) is an important mechanism for the repair of damaged chromosomes, for preventing the demise of damaged replication forks, and for several other aspects of chromosome maintenance. As such, HR is indispensable for genome integrity, but it must be regulated to avoid deleterious events. Mutations in the tumour-suppressor protein BRCA2, which has a mediator function in HR, lead to cancer formation. DNA helicases, such as Bloom's syndrome protein (BLM), regulate HR at several levels, in attenuating unwanted HR events and in determining the outcome of HR. Defects in BLM are also associated with the cancer phenotype. The past several years have witnessed dramatic advances in our understanding of the mechanism and regulation of HR.
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U2 - 10.1038/nrm2008
DO - 10.1038/nrm2008
M3 - Review article
C2 - 16926856
AN - SCOPUS:33749037701
SN - 1471-0072
VL - 7
SP - 739
EP - 750
JO - Nature Reviews Molecular Cell Biology
JF - Nature Reviews Molecular Cell Biology
IS - 10
ER -