TY - JOUR
T1 - Suffering in silence
T2 - The tolerance of DNA damage
AU - Friedberg, Errol C.
N1 - Funding Information:
I thank S. Squires, P. Fischhaber, L. McDaniel, R. Schultz, N. Kosarek, G. Walker and W. Siede for critical review of the manuscript and helpful discussions. Work in my laboratory is supported by a research grant from the United States Public Health Service (USPHS).
PY - 2005/12
Y1 - 2005/12
N2 - When cells that are actively replicating DNA encounter sites of base damage or strand breaks, replication might stall or arrest. In this situation, cells rely on DNA-damage-tolerance mechanisms to bypass the damage effectively. One of these mechanisms, known as translesion DNA synthesis, is supported by specialized DNA polymerases that are able to catalyse nucleotide incorporation opposite lesions that cannot be negotiated by high-fidelity replicative polymerases. A second category of tolerance mechanism involves alternative replication strategies that obviate the need to replicate directly across sites of template-strand damage.
AB - When cells that are actively replicating DNA encounter sites of base damage or strand breaks, replication might stall or arrest. In this situation, cells rely on DNA-damage-tolerance mechanisms to bypass the damage effectively. One of these mechanisms, known as translesion DNA synthesis, is supported by specialized DNA polymerases that are able to catalyse nucleotide incorporation opposite lesions that cannot be negotiated by high-fidelity replicative polymerases. A second category of tolerance mechanism involves alternative replication strategies that obviate the need to replicate directly across sites of template-strand damage.
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U2 - 10.1038/nrm1781
DO - 10.1038/nrm1781
M3 - Review article
C2 - 16341080
AN - SCOPUS:28844506236
SN - 1471-0072
VL - 6
SP - 943
EP - 953
JO - Nature Reviews Molecular Cell Biology
JF - Nature Reviews Molecular Cell Biology
IS - 12
ER -