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PCNA, the Maestro of the Replication Fork
Open accessAbstract
Inheritance requires genome duplication, reproduction of chromatin and its epigenetic information, mechanisms to ensure genome integrity, and faithful transmission of the information to progeny. Proliferating cell nuclear antigen (PCNA)-a cofactor of DNA polymerases that encircles DNA-orchestrates several of these functions by recruiting crucial players to the replication fork. Remarkably, many factors that are involved in replication-linked processes interact with a particular face of PCNA and through the same interaction domain, indicating that these interactions do not occur simultaneously during replication. Switching of PCNA partners may be triggered by affinity-driven competition, phosphorylation, proteolysis, and modification of PCNA by ubiquitin and SUMO.
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“And, although PCNA is a crucial component of the replication fork during the cell cycle, it also functions in DNA repair.167”
From Census and evaluation of p53 target genes (2017) · cites this paper as [167]
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Gazy, I., Liefshitz, B., Parnas, O., & Kupiec, M. (2014) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2014.11.007 · Cited by 15
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Metadata
- Authors
- Moldovan, G.-L., Pfander, B., & Jentsch, S.
- Affiliations
- Harvard University (US)
- Cancer Research UK (GB)
- Max Planck Institute of Biochemistry (DE)
- Corresponding author
- Jentsch, Stefan
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 129
- Issue
- 4
- Pages
- 665-679
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2072747624
- Cited by
- 1,796
- References
- 110
- Citations by year
- 2026: 53 · 2025: 70 · 2024: 77 · 2023: 84 · 2022: 80 · 2021: 86 · 2020: 87 · 2019: 97 · 2018: 87 · 2017: 111 · 2016: 113 · 2015: 92 · 2014: 113 · 2013: 106 · 2012: 125
- FWCI
- 8.35
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 2269 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Max Planck Institute for Plasma Physics (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- proliferating cell nuclear antigen, PCNA, DNA replication, replication fork, genome stability, epigenetic inheritance, whole-genome duplication, protein-protein interaction, phosphorylation, ubiquitination, SUMOylation, proteolysis, chromatin inheritance
- MeSH terms
- Animals, DNA-Directed DNA Polymerase, DNA Repair, DNA Replication, DNA-Binding Proteins, Humans, S Phase, Cell Cycle Proteins, Proliferating Cell Nuclear Antigen, Genomic Instability, Epigenesis, Genetic
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