ArticleNature communications2014
HSP90 regulates DNA repair via the interaction between XRCC1 and DNA polymerase β.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
74 citing papers in PubMed, 111 citations in OpenAlex.
- GCN5 and TADA2B constitutively regulate XRCC1 function during DNA repair to maintain cell survival.Cell death and differentiation · 2026Article
- HSF1 and YTHDC1 enhance DNA repair under heat stress by promoting repair-associated gene expression.Nucleic acids research · 2026Article
- Ubiquitylation of DNA polymerase β via atypical K27 chains signals a DNA damage response.Nucleic acids research · 2026Article
- Hypomorphic Protein Expression of DNA Polymerase Beta in PolβBiomolecules · 2026Article
- Envafolimab - novel anti-PD-1/PD-L1 antibody in cancer treatment.Frontiers in immunology · 2026Review
- Replication-associated base excision repair/single-strand break repair regulates PARG inhibitor response via the PRMT1/PRMT5/ATR axis.NAR cancer · 2025Article
- TRIP12's role in the governance of DNA polymerase β involvement in DNA damage response and repair.Nucleic acids research · 2025Article
- Protein-Protein Interactions in Base Excision Repair.Biomolecules · 2025Review
- Overexpression of the WWE domain of RNF146 modulates poly-(ADP)-ribose dynamics at sites of DNA damage.DNA repair · 2025Article
- DNA polymerase beta expression in head & neck cancer modulates the poly(ADP-ribose)-mediated replication checkpoint.DNA repair · 2025Article
- Temperature Is a Key Factor Governing the Toxic Impact of Ultra-Violet Radiation-Emitting Nail Dryers When Used on Human Skin Cells.International journal of toxicology · 2024Article
- Article
- Mouse models to explore the biological and organismic role of DNA polymerase beta.Environmental and molecular mutagenesis · 2024Review
- Hsp90-Mediated Multi-Drug Resistance in DNA Polymerase-Defective Strains ofJournal of fungi (Basel, Switzerland) · 2024Article
- Impact of polβ/XRCC1 Interaction Variants on the Efficiency of Nick Sealing by DNA Ligase IIIα in the Base Excision Repair Pathway.Journal of molecular biology · 2024Article
- Disabled-2: a protein up-regulated by high molecular weight hyaluronan has both tumor promoting and tumor suppressor roles in ovarian cancer.Cellular and molecular life sciences : CMLS · 2023Article
- Potent antitumor efficacy of human dental pulp stem cells armed with YSCH-01 oncolytic adenovirus.Journal of translational medicine · 2023Article
- A multi-scale map of protein assemblies in the DNA damage response.Cell systems · 2023Article
- Polβ/XRCC1 heterodimerization dictates DNA damage recognition and basal Polβ protein levels without interfering with mouse viability or fertility.DNA repair · 2023Article
- Integrated Transcriptome and Metabolome Analysis to Identify Sugarcane Gene Defense against Fall Armyworm (International journal of molecular sciences · 2022Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Cellular DNA repair processes are crucial to maintain genome stability and integrity. In DNA base excision repair, a tight heterodimer complex formed by DNA polymerase β (Polβ) and XRCC1 is thought to facilitate repair by recruiting Polβ to DNA damage sites. Here we show that disruption of the complex does not impact DNA damage response or DNA repair. Instead, the heterodimer formation is required to prevent ubiquitylation and degradation of Polβ. In contrast, the stability of the XRCC1 monomer is protected from CHIP-mediated ubiquitylation by interaction with the binding partner HSP90. In response to cellular proliferation and DNA damage, proteasome and HSP90-mediated regulation of Polβ and XRCC1 alters the DNA repair complex architecture. We propose that protein stability, mediated by DNA repair protein complex formation, functions as a regulatory mechanism for DNA repair pathway choice in the context of cell cycle progression and genome surveillance.
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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.