
doi: 10.1038/nrm1907 , 10.5167/uzh-34288
pmid: 16612326
By removing biosynthetic errors from newly synthesized DNA, mismatch repair (MMR) improves the fidelity of DNA replication by several orders of magnitude. Loss of MMR brings about a mutator phenotype, which causes a predisposition to cancer. But MMR status also affects meiotic and mitotic recombination, DNA-damage signalling, apoptosis and cell-type-specific processes such as class-switch recombination, somatic hypermutation and triplet-repeat expansion. This article reviews our current understanding of this multifaceted DNA-repair system in human cells.
Exonucleases, Models, Molecular, DNA Repair, Base Pair Mismatch, 10061 Institute of Molecular Cancer Research, Drug Resistance, 1307 Cell Biology, Proliferating Cell Nuclear Antigen, 1312 Molecular Biology, Animals, Humans, 570 Life sciences; biology
Exonucleases, Models, Molecular, DNA Repair, Base Pair Mismatch, 10061 Institute of Molecular Cancer Research, Drug Resistance, 1307 Cell Biology, Proliferating Cell Nuclear Antigen, 1312 Molecular Biology, Animals, Humans, 570 Life sciences; biology
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