ArticleThe Journal of biological chemistry2009
Long patch base excision repair proceeds via coordinated stimulation of the multienzyme DNA repair complex.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 60 citations in OpenAlex.
- Hypomorphic Protein Expression of DNA Polymerase Beta in PolβBiomolecules · 2026Article
- Mechanisms underlying low mutation rates in mammalian oocytes and preimplantation embryos.Nucleic acids research · 2025Review
- Single-molecule studies of repair proteins in base excision repair.BMB reports · 2025Review
- Harnessing DNA polymerase beta defect enhances synthetic lethality and treatment response in gastric cancer cells: implication for immunotherapy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2025Review
- Human CST Stimulates Base Excision Repair to Prevent the Accumulation of Oxidative DNA Damage.Journal of molecular biology · 2024Article
- DNA Damage and Repair in Eye Diseases.International journal of molecular sciences · 2023Review
- Using Affinity Pulldown Assays to Study Protein-Protein Interactions of Human NEIL1 Glycosylase and the Checkpoint Protein RAD9-RAD1-HUS1 (9-1-1) Complex.Methods in molecular biology (Clifton, N.J.) · 2023Article
- FOXP1 and NDRG1 act differentially as downstream effectors of RAD9-mediated prostate cancer cell functions.Cellular signalling · 2021Article
- Targeted DNA oxidation by LSD1-SMAD2/3 primes TGF-β1/ EMT genes for activation or repression.Nucleic acids research · 2020Article
- Acetylation and Deacetylation of DNA Repair Proteins in Cancers.Frontiers in oncology · 2020Review
- Prostate cancer: unmet clinical needs and RAD9 as a candidate biomarker for patient management.Translational cancer research · 2018Article
- Article
- p53 and RAD9, the DNA Damage Response, and Regulation of Transcription Networks.Radiation research · 2017Review
- Bringing It All Together: Coupling Excision Repair to the DNA Damage Checkpoint.Photochemistry and photobiology · 2017Review
- Rate-determining Step of Flap Endonuclease 1 (FEN1) Reflects a Kinetic Bias against Long Flaps and Trinucleotide Repeat Sequences.The Journal of biological chemistry · 2015Article
- New paradigms in the repair of oxidative damage in human genome: mechanisms ensuring repair of mutagenic base lesions during replication and involvement of accessory proteins.Cellular and molecular life sciences : CMLS · 2015Review
- A chemical and kinetic perspective on base excision repair of DNA.Accounts of chemical research · 2014Article
- Opening pathways of the DNA clamps proliferating cell nuclear antigen and Rad9-Rad1-Hus1.Nucleic acids research · 2013Article
- Article
- Understanding the role of the Q338H MUTYH variant in oxidative damage repair.Nucleic acids research · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Base excision repair, a major repair pathway in mammalian cells, is responsible for correcting DNA base damage and maintaining genomic integrity. Recent reports show that the Rad9-Rad1-Hus1 complex (9-1-1) stimulates enzymes proposed to perform a long patch-base excision repair sub-pathway (LP-BER), including DNA glycosylases, apurinic/apyrimidinic endonuclease 1 (APE1), DNA polymerase beta (pol beta), flap endonuclease 1 (FEN1), and DNA ligase I (LigI). However, 9-1-1 was found to produce minimal stimulation of FEN1 and LigI in the context of a complete reconstitution of LP-BER. We show here that pol beta is a robust stimulator of FEN1 and a moderate stimulator of LigI. Apparently, there is a maximum possible stimulation of these two proteins such that after responding to pol beta or another protein in the repair complex, only a small additional response to 9-1-1 is allowed. The 9-1-1 sliding clamp structure must serve primarily to coordinate enzyme actions rather than enhancing rate. Significantly, stimulation by the polymerase involves interaction of primer terminus-bound pol beta with FEN1 and LigI. This observation provides compelling evidence that the proposed LP-BER pathway is actually employed in cells. Moreover, this pathway has been proposed to function by sequential enzyme actions in a "hit and run" mechanism. Our results imply that this mechanism is still carried out, but in the context of a multienzyme complex that remains structurally intact during the repair process.
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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.