{"doi":"10.1042/bj20030491","title":"RecQ helicases: suppressors of tumorigenesis and premature aging","abstract":"<jats:p>The RecQ helicases represent a subfamily of DNA helicases that are highly conserved in evolution. Loss of RecQ helicase function leads to a breakdown in the maintenance of genome integrity, in particular hyper-recombination. Germ-line defects in three of the five known human RecQ helicases give rise to defined genetic disorders associated with cancer predisposition and/or premature aging. These are Bloom's syndrome, Werner's syndrome and Rothmund–Thomson syndrome, which are caused by defects in the genes BLM, WRN and RECQ4 respectively. Here we review the properties of RecQ helicases in organisms from bacteria to humans, with an emphasis on the biochemical functions of these enzymes and the range of protein partners that they operate with. We will discuss models in which RecQ helicases are required to protect against replication fork demise, either through prevention of fork breakdown or restoration of productive DNA synthesis.</jats:p>","journal":"Biochemical Journal","year":2003,"id":688949,"datarank":0.8882367629465725,"base_score":5.921578419643816,"endowment":5.921578419643816,"self_citation_contribution":0.8882367629465725,"citation_network_contribution":0.0,"self_endowment_contribution":0.8882367629465725,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":372,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":6,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":1799868,"name":"Ian D. HICKSON","orcid":null,"position":1,"is_corresponding":false},{"id":1799867,"name":"Csanád Z. BACHRATI","orcid":null,"position":0,"is_corresponding":false}],"reference_count":0,"raw_metadata":{"has_enrichment":true,"resolved":true,"title":"RecQ helicases: suppressors of tumorigenesis and premature aging","abstract":"<jats:p>The RecQ helicases represent a subfamily of DNA helicases that are highly conserved in evolution. Loss of RecQ helicase function leads to a breakdown in the maintenance of genome integrity, in particular hyper-recombination. Germ-line defects in three of the five known human RecQ helicases give rise to defined genetic disorders associated with cancer predisposition and/or premature aging. These are Bloom's syndrome, Werner's syndrome and Rothmund–Thomson syndrome, which are caused by defects in the genes BLM, WRN and RECQ4 respectively. Here we review the properties of RecQ helicases in organisms from bacteria to humans, with an emphasis on the biochemical functions of these enzymes and the range of protein partners that they operate with. We will discuss models in which RecQ helicases are required to protect against replication fork demise, either through prevention of fork breakdown or restoration of productive DNA synthesis.</jats:p>","is_dataset_classified":null,"base_score":5.921578419643816,"endowment":5.921578419643816,"datacite_reuse_total":6,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"12803543","pmcid":"PMC1223634","openalex_id":"https://openalex.org/W2025180999","authors":[],"funders":[],"total_grants":0,"fwci":11.8104,"citation_percentile":0.99258784,"influential_citations":0,"citation_trend":[{"year":2012,"count":15},{"year":2013,"count":9},{"year":2014,"count":24},{"year":2015,"count":10},{"year":2016,"count":5},{"year":2017,"count":7},{"year":2018,"count":8},{"year":2019,"count":8},{"year":2020,"count":7},{"year":2021,"count":5},{"year":2022,"count":6},{"year":2023,"count":6},{"year":2024,"count":8},{"year":2025,"count":5}],"oa_status":"bronze","license":null,"oa_locations":[{"url":"https://portlandpress.com/biochemj/article-pdf/374/3/577/711716/bj3740577.pdf","host_type":"journal"},{"url":"https://portlandpress.com/biochemj/article-pdf/374/3/577/711716/bj3740577.pdf","host_type":"publisher"},{"url":"https://doi.org/10.1042/bj20030491","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/12803543","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/1223634","host_type":"repository"}],"fields_of_study":["DNA Repair Mechanisms","Carcinogens and Genotoxicity Assessment","Plant Genetic and Mutation Studies","Adenosine Triphosphatases","Aging, Premature","Animals","DNA Helicases","Genes, Tumor Suppressor","Genetic Predisposition to Disease","Humans","Mutation","Neoplasms","RecQ Helicases"],"mesh_terms":["Adenosine Triphosphatases","Animals","DNA Helicases","Humans","Mutation","Neoplasms","Genes, Tumor Suppressor","Aging, Premature","Genetic Predisposition to Disease","RecQ Helicases"],"keywords":["Helicase","RecQ helicase","Werner syndrome","Biology","Genetics","Bloom syndrome","Premature aging","Genome instability","DNA repair","DNA","DNA damage","Gene"],"sdg_mappings":[],"linked_datasets":[{"doi":"10.6084/m9.figshare.26607349.v1","title":"Additional file 1 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.26607349","title":"Additional file 1 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.26607355.v1","title":"Additional file 3 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.26607355","title":"Additional file 3 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"JournalArticle"},{"doi":"10.6084/m9.figshare.26607352.v1","title":"Additional file 2 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"Dataset"},{"doi":"10.6084/m9.figshare.26607352","title":"Additional file 2 of TRIM58 functions as a tumor suppressor in colorectal cancer by promoting RECQL4 ubiquitination to inhibit the AKT signaling pathway","publisher":"figshare","resource_type":"Dataset"}],"clinical_trials":[],"software_tools":[],"database_accessions":[],"source":"live","citation_network_status":"fetched"},"created_at":"2026-08-19T20:46:08.071790Z","pmid":null,"pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}