ArticleMolecular and cellular biology2010
Replication factor C recruits DNA polymerase delta to sites of nucleotide excision repair but is not required for PCNA recruitment.
Article in Molecular and cellular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 67 citations in OpenAlex.
- A DLBCL Prognostic model superior to the IPI score: Mechanistic study and clinical validation based on RFC2- and RFC4-mediated DNA damage repair.Clinical and experimental medicine · 2026Article
- The impact of Iso-mukaadial acetate on Plasmodium falciparum transcriptional gene regulation.Scientific reports · 2025Article
- Proteomic discovery of DEK and NUMA1 as new players in UV-induced DNA damage repair mechanisms.Cell death discovery · 2025Article
- RFC1 regulates the expansion of neural progenitors in the developing zebrafish cerebellum.Nature communications · 2025Article
- From the Cytoplasm into the Nucleus-Hepatitis B Virus Travel and Genome Repair.Microorganisms · 2025Review
- Cockayne syndrome B protein is implicated in transcription and associated chromatin dynamics in homeostatic and genotoxic conditions.Aging cell · 2025Article
- AAGGG repeat expansions triggerScience advances · 2024Article
- The type of DNA damage response after decitabine treatment depends on the level of DNMT activity.Life science alliance · 2024Article
- K48- and K63-linked ubiquitin chain interactome reveals branch- and length-specific ubiquitin interactors.Life science alliance · 2024Article
- Enhanced frequency of transcription pre-initiation complexes assembly after exposure to UV irradiation results in increased repair activity and reduced probabilities for mutagenesis.Nucleic acids research · 2023Article
- Unexpected new insights into DNA clamp loaders: Eukaryotic clamp loaders contain a second DNA site for recessed 5' ends that facilitates repair and signals DNA damage: Eukaryotic clamp loaders contain a second DNA site for recessed 5' ends that facilitates repair and signals DNA damage.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
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- Recessive cerebellar and afferent ataxias - clinical challenges and future directions.Nature reviews. Neurology · 2022Review
- Active DNA damage eviction by HLTF stimulates nucleotide excision repair.Molecular cell · 2022Article
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- aniFOUND: analysing the associated proteome and genomic landscape of the repaired nascent non-replicative chromatin.Nucleic acids research · 2021Article
- Polymerase δ promotes chromosomal rearrangements and imprecise double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- ShRNA-based POLD2 expression knockdown sensitizes glioblastoma to DNA-Damaging therapeutics.Cancer letters · 2020Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nucleotide excision repair (NER) operates through coordinated assembly of repair factors into pre- and postincision complexes. The postincision step of NER includes gap-filling DNA synthesis and ligation. However, the exact composition of this NER-associated DNA synthesis complex in vivo and the dynamic interactions of the factors involved are not well understood. Using immunofluorescence, chromatin immunoprecipitation, and live-cell protein dynamic studies, we show that replication factor C (RFC) is implicated in postincision NER in mammalian cells. Small interfering RNA-mediated knockdown of RFC impairs upstream removal of UV lesions and abrogates the downstream recruitment of DNA polymerase delta. Unexpectedly, RFC appears dispensable for PCNA recruitment yet is required for the subsequent recruitment of DNA polymerases to PCNA, indicating that RFC is essential to stably load the polymerase clamp to start DNA repair synthesis at 3' termini. The kinetic studies are consistent with a model in which RFC exchanges dynamically at sites of repair. However, its persistent localization at stalled NER complexes suggests that RFC remains targeted to the repair complex even after loading of PCNA. We speculate that RFC associates with the downstream 5' phosphate after loading; such interaction would prevent possible signaling events initiated by the RFC-like Rad17 and may assist in unloading of PCNA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.