ArticleMechanisms of ageing and development2010
WRN participates in translesion synthesis pathway through interaction with NBS1.
Article in Mechanisms of ageing and development, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Implication of E3 ligase RAD18 in UV-induced mutagenesis in human induced pluripotent stem cells and neuronal progenitor cells.Journal of radiation research · 2023Article
- Post-Translational Modifications of PCNA in Control of DNA Synthesis and DNA Damage Tolerance-the Implications in Carcinogenesis.International journal of biological sciences · 2021Review
- Nucleolar protein nucleolin functions in replication stress-induced DNA damage responses.Journal of radiation research · 2019Article
- Werner Syndrome Protein and DNA Replication.International journal of molecular sciences · 2018Review
- Replication stress induced site-specific phosphorylation targets WRN to the ubiquitin-proteasome pathway.Oncotarget · 2016Article
- RECQ helicases are deregulated in hematological malignancies in association with a prognostic value.Biomarker research · 2016Article
- Envisioning the dynamics and flexibility of Mre11-Rad50-Nbs1 complex to decipher its roles in DNA replication and repair.Progress in biophysics and molecular biology · 2015Review
- Nonenzymatic role for WRN in preserving nascent DNA strands after replication stress.Cell reports · 2014Article
- Targeting an Achilles' heel of cancer with a WRN helicase inhibitor.Cell cycle (Georgetown, Tex.) · 2013Article
- Nucleolin participates in DNA double-strand break-induced damage response through MDC1-dependent pathway.PloS one · 2012Article
- DNA repair deficiency in neurodegeneration.Progress in neurobiology · 2011Review
- Mechanism of cluster DNA damage repair in response to high-atomic number and energy particles radiation.Mutation research · 2011Review
- Mre11-Rad50-Nbs1 conformations and the control of sensing, signaling, and effector responses at DNA double-strand breaks.DNA repair · 2010Review
- Cellular deficiency of Werner syndrome protein or RECQ1 promotes genotoxic potential of hydroquinone and benzo[a]pyrene exposure.International journal of toxicologyArticle
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
Abstract
Werner syndrome (WS), caused by mutation of the WRN gene, is an autosomal recessive disorder associated with premature aging and predisposition to cancer. WRN belongs to the RecQ DNA helicase family, members of which play a role in maintaining genomic stability. Here, we demonstrate that WRN rapidly forms discrete nuclear foci in an NBS1-dependent manner following DNA damage. NBS1 physically interacts with WRN through its FHA domain, which interaction is important for the phosphorylation of WRN. WRN subsequently forms DNA damage-dependent foci during the S phase, but not in the G1 phase. WS cells exhibit an increase in spontaneous focus formation of poleta and Rad18, which are important for translesion synthesis (TLS). WRN also interacts with PCNA in the absence of DNA damage, but DNA damage induces the dissociation of PCNA from WRN, leading to the ubiquitination of PCNA, which is essential for TLS. This dissociation correlates with ATM/NBS1-dependent degradation of WRN. Moreover, WS cells show constitutive ubiquitination of PCNA and interaction between PCNA and Rad18 E3 ligase in the absence of DNA damage. Taken together, these results indicate that WRN participates in the TLS pathway to prevent genomic instability in an ATM/NBS1-dependent manner.
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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.