ArticleOncogene2001
Diverged nuclear localization of Werner helicase in human and mouse cells.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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.
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Who cites it
28 citing papers in PubMed, 66 citations in OpenAlex.
- SNORD88B-mediated WRN nucleolar trafficking drives self-renewal in liver cancer initiating cells and hepatocarcinogenesis.Nature communications · 2024Article
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- The identification of a novel mutation (p.I223fs) in WRN associated with Werner syndrome.Endocrine · 2024Article
- Werner syndrome in a Lebanese family.American journal of medical genetics. Part A · 2022Article
- Article
- Human RecQ Helicases in DNA Double-Strand Break Repair.Frontiers in cell and developmental biology · 2021Review
- Acetylation of Werner protein at K1127 and K1117 is important for nuclear trafficking and DNA repair.DNA repair · 2019Article
- WRN Mutation Update: Mutation Spectrum, Patient Registries, and Translational Prospects.Human mutation · 2017Review
- Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions.Ageing research reviews · 2017Review
- Article
- Ethnic-Specific WRN Mutations in South Asian Werner Syndrome Patients: Potential Founder Effect in Patients with Indian or Pakistani Ancestry.Molecular genetics & genomic medicine · 2013Article
- DNA helicases associated with genetic instability, cancer, and aging.Advances in experimental medicine and biology · 2013Article
- Hereditary nonmelanoma skin cancer.Seminars in cutaneous medicine and surgery · 2012Review
- Article
- WRN mutations in Werner syndrome patients: genomic rearrangements, unusual intronic mutations and ethnic-specific alterations.Human genetics · 2010Article
- Bypassing cellular senescence by genetic screening tools.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2010Review
- The Nucleolus Takes Control of Protein Trafficking Under Cellular Stress.Molecular and cellular pharmacology · 2010Article
- The Werner syndrome protein functions in repair of Cr(VI)-induced replication-associated DNA damage.Toxicological sciences : an official journal of the Society of Toxicology · 2009Article
- Human Wrnip1 is localized in replication factories in a ubiquitin-binding zinc finger-dependent manner.The Journal of biological chemistry · 2008Article
- The clinical characteristics of Werner syndrome: molecular and biochemical diagnosis.Human genetics · 2008Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Werner syndrome (WS) is a rare autosomal recessive genetic disorder causing premature aging and rare cancers. A gene responsible for WS (WRN) encodes a protein with 1432 amino acids (a.a.) homologous to the E. coli RecQ-type DNA helicase. Transcriptional activation facilitated nucleolar localization of human WRN protein (hWRNp) and serum starvation induced translocation of hWRNp from the nucleoli to the nucleoplasm in human cultured cells, suggesting a nucleolar-nucleoplasm trafficking of hWRNp depending on transcriptional state. Mutant hWRNp lacking the C-terminal 30 a.a. residues (Delta1403-1432) failed to localize in the nucleolus, whereas Delta1405-1432 can migrate into the nucleolus. Here we identify a region putative for nucleolar localization signal (NoLS) containing a sequence of two positively charged amino acids (Arg(1403)-Lys(1404)) in the C-terminal area of hWRNp. By contrast, the mouse homolog (mWRNp) exists only in the nucleoplasm. We show that the inability of mWRNp to migrate into the nucleolus is due to a difference of a sequence in the region corresponding to the NoLS of hWRNp. In addition, mouse cells cannot recognize the NoLS of hWRNp. Our study suggests that defect in nucleolar function of hWRNp may be linked to the premature aging which is not observed in mWRN(-/-) mice.
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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.