ArticleOncogene2014
K63-ubiquitylation of VHL by SOCS1 mediates DNA double-strand break repair.
Article in Oncogene, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Study of inborn errors of immunity associated lymphoid proliferations identifies association of presence of somatic variations with large cell morphology, copy number alterations in TNFAIP3 and heterozygous variants in EMSY.Virchows Archiv : an international journal of pathology · 2026Article
- Von Hippel-Lindau disease: pathophysiological and clinical advances.Familial cancer · 2026Review
- Essential genetic mutations impair DNA damage repair and modulate tumor immune microenvironment in ccRCC.MedScience · 2026Review
- Tumor-initiating and metastasis-initiating cells of clear-cell renal cell carcinoma.Journal of biomedical science · 2025Review
- The Fanconi anemia core complex promotes CtIP-dependent end resection to drive homologous recombination at DNA double-strand breaks.Nature communications · 2024Article
- Article
- Role of K63-linked ubiquitination in cancer.Cell death discovery · 2022Review
- Genome-wide CRISPR screens using isogenic cells reveal vulnerabilities conferred by loss of tumor suppressors.Science advances · 2022Article
- Review
- IQGAP3 in clear cell renal cell carcinoma contributes to drug resistance and genome stability.PeerJ · 2022Article
- A genomic instability-derived risk index predicts clinical outcome and immunotherapy response for clear cell renal cell carcinoma.Bioengineered · 2021Article
- E3 ligase TRIM25 ubiquitinates RIP3 to inhibit TNF induced cell necrosis.Cell death and differentiation · 2021Article
- Clear cell renal cell carcinoma ontogeny and mechanisms of lethality.Nature reviews. Nephrology · 2021Review
- Zebrafish Cancer Predisposition Models.Frontiers in cell and developmental biology · 2021Review
- LINC00671 inhibits renal cell cancer progression via regulating miR-221-5p/SOCS1 axis.American journal of translational research · 2021Article
- The long form of pVHL is artifactually modified by serine protease inhibitor AEBSF.Protein science : a publication of the Protein Society · 2020Article
- Investigation of the role of VHL-HIF signaling in DNA repair and apoptosis in zebrafish.Oncotarget · 2020Article
- Suppression of the Ubiquitin Pathway by Small Molecule Binding to Ubiquitin Enhances Doxorubicin Sensitivity of the Cancer Cells.Molecules (Basel, Switzerland) · 2019Article
- Disturbed Flow Increases UBE2C (Ubiquitin E2 Ligase C) via Loss of miR-483-3p, Inducing Aortic Valve Calcification by the pVHL (von Hippel-Lindau Protein) and HIF-1α (Hypoxia-Inducible Factor-1α) Pathway in Endothelial Cells.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Cullin 5 is a novel candidate tumor suppressor in renal cell carcinoma involved in the maintenance of genome stability.Oncogenesis · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
DNA repair is essential for maintaining genomic stability, and defects in this process significantly increase the risk of cancer. Clear-cell renal cell carcinoma (CCRCC) caused by inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene is characterized by high genomic instability. However, the molecular mechanism underlying the association between the loss of VHL and genomic instability remains unclear. Here, we show that suppressor of cytokine signaling 1 (SOCS1) promotes nuclear redistribution and K63-ubiquitylation of VHL in response to DNA double-strand breaks (DSBs). Loss of VHL or VHL mutations that compromise its K63-ubiquitylation attenuates the DNA-damage response (DDR), resulting in decreased homologous recombination repair and persistence of DSBs. These results identify VHL as a component of the DDR network, inactivation of which contributes to the genomic instability associated with CCRCC.
Indexed as
Identifiers
What OpenQuestion holds
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.