ArticleBiochemistry2013
Distinct structural alterations in proliferating cell nuclear antigen block DNA mismatch repair.
Article in Biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed.
- CAF-1 in Replication and Repair: A Critical Genetic Mediator of Synthesis-Coupled Nucleosome Assembly.Biomolecules · 2026Review
- Lagging strand gap suppression connects BRCA-mediated fork protection to nucleosome assembly through PCNA-dependent CAF-1 recycling.Nature communications · 2022Article
- Article
- Discovery of Inhibitors for Proliferating Cell Nuclear Antigen Using a Computational-Based Linked-Multiple-Fragment Screen.ACS omega · 2019Article
- Effective mismatch repair depends on timely control of PCNA retention on DNA by the Elg1 complex.Nucleic acids research · 2019Article
- Article
- PCNA Retention on DNA into G2/M Phase Causes Genome Instability in Cells Lacking Elg1.Cell reports · 2016Article
- The Proliferating Cell Nuclear Antigen (PCNA)-interacting Protein (PIP) Motif of DNA Polymerase η Mediates Its Interaction with the C-terminal Domain of Rev1.The Journal of biological chemistry · 2016Article
- Dead-End Elimination with a Polarizable Force Field Repacks PCNA Structures.Biophysical journal · 2015Article
- PCNA and Msh2-Msh6 activate an Mlh1-Pms1 endonuclease pathway required for Exo1-independent mismatch repair.Molecular cell · 2014Article
- Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
During DNA replication, mismatches and small loops in the DNA resulting from insertions or deletions are repaired by the mismatch repair (MMR) machinery. Proliferating cell nuclear antigen (PCNA) plays an important role in both mismatch-recognition and resynthesis stages of MMR. Previously, two mutant forms of PCNA were identified that cause defects in MMR with little, if any, other defects. The C22Y mutant PCNA protein completely blocks MutSα-dependent MMR, and the C81R mutant PCNA protein partially blocks both MutSα-dependent and MutSβ-dependent MMR. In order to understand the structural and mechanistic basis by which these two amino acid substitutions in PCNA proteins block MMR, we solved the X-ray crystal structures of both mutant proteins and carried out further biochemical studies. We found that these amino acid substitutions lead to subtle, distinct structural changes in PCNA. The C22Y substitution alters the positions of the α-helices lining the central hole of the PCNA ring, whereas the C81R substitution creates a distortion in an extended loop near the PCNA subunit interface. We conclude that the structural integrity of the α-helices lining the central hole and this loop are both necessary to form productive complexes with MutSα and mismatch-containing DNA.
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