ArticleCell reports2015
UHRF1 contributes to DNA damage repair as a lesion recognition factor and nuclease scaffold.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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The trial behind it
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Who cites it
65 citing papers in PubMed, 98 citations in OpenAlex.
- Eprenetapopt in combination with Palbociclib exerts synthetic lethality in mantle cell lymphoma.Translational oncology · 2026Article
- Reduced Maintenance DNA Methylation Thresholds Enable Sensitive Reporter Assays for UHRF1 and DNMT1 Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- UHRF1 deficiency exacerbates intestinal inflammation by epigenetic modulation of NPY1R gene methylation.JCI insight · 2026Article
- Mutagenic Potentials of DNA Interstrand Cross-Links Induced by 7,8-Dihydro-8-Oxoadenine.Molecules (Basel, Switzerland) · 2026Article
- UHRF1 Controls the Timing of RAD51 Removal During DNA Damage Repair Through Suppressing RFWD3.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- UHRF1 in endothelial cells is essential for angiogenesis and associated with the activation of pro-angiogenic signaling pathways and expression of endothelial genes.Angiogenesis · 2025Article
- CIT kinase phosphorylation as significant regulatory node for cellular checkpoints.Frontiers in bioinformatics · 2025Article
- RAD51 plays critical roles in DNMT1-mediated maintenance methylation of genomic DNA by dually regulating the ubiquitin ligase UHRF1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Aberrant cytoplasmic expression of UHRF1 restrains the MHC-I-mediated anti-tumor immune response.Nature communications · 2024Article
- Non-canonical functions of UHRF1 maintain DNA methylation homeostasis in cancer cells.Nature communications · 2024Article
- AMPK activation attenuates central sensitization in a recurrent nitroglycerin-induced chronic migraine mouse model by promoting microglial M2-type polarization.The journal of headache and pain · 2024Article
- Natural and Synthetic Anticancer Epidrugs Targeting the Epigenetic Integrator UHRF1.Molecules (Basel, Switzerland) · 2023Review
- UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma.Nature communications · 2023Article
- Inhibition of Protein Disulfide Isomerase (PDIA1) Leads to Proteasome-Mediated Degradation of Ubiquitin-like PHD and RING Finger Domain-Containing Protein 1 (UHRF1) and Increased Sensitivity of Glioblastoma Cells to Topoisomerase II Inhibitors.ACS pharmacology & translational science · 2023Article
- Molecular basis of hUHRF1 allosteric activation for synergistic histone modification binding by PI5P.Science advances · 2022Article
- DNA Damage Response Regulation by Histone Ubiquitination.International journal of molecular sciences · 2022Review
- PWWP2B promotes DNA end resection and homologous recombination.EMBO reports · 2022Article
- Genome maintenance in retinoblastoma: Implications for therapeutic vulnerabilities.Oncology letters · 2022Review
- Epigenetic regulator UHRF1 orchestrates proinflammatory gene expression in rheumatoid arthritis in a suppressive manner.The Journal of clinical investigation · 2022Article
- Nuclear UHRF1 is a gate-keeper of cellular AMPK activity and function.Cell research · 2022Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
We identified ubiquitin-like with PHD and RING finger domain 1 (UHRF1) as a binding factor for DNA interstrand crosslink (ICL) lesions through affinity purification of ICL-recognition activities. UHRF1 is recruited to DNA lesions in vivo and binds directly to ICL-containing DNA. UHRF1-deficient cells display increased sensitivity to a variety of DNA damages. We found that loss of UHRF1 led to retarded lesion processing and reduced recruitment of ICL repair nucleases to the site of DNA damage. UHRF1 interacts physically with both ERCC1 and MUS81, two nucleases involved in the repair of ICL lesions. Depletion of both UHRF1 and components of the Fanconi anemia (FA) pathway resulted in increased DNA damage sensitivity compared to defect of each mechanism alone. These results suggest that UHRF1 promotes recruitment of lesion-processing activities via its affinity to recognize DNA damage and functions as a nuclease recruitment scaffold in parallel to the FA pathway.
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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.