ReviewOncogene2002
RecQ family helicases: roles as tumor suppressor proteins.
Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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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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.
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Who cites it
29 citing papers in PubMed, 82 citations in OpenAlex.
- Novel mutations in the RECQL4 gene affect its helicase functions, interactions with the BLM helicase and chemotherapeutics-induced cell death.Cell death discovery · 2025Article
- Congenital Telangiectatic Erythema: Scoping Review.JMIR dermatology · 2023Article
- Breast cancer patients suggestive of Li-Fraumeni syndrome: mutational spectrum, candidate genes, and unexplained heredity.Breast cancer research : BCR · 2018Article
- Functional and evolutionary analysis of viral proteins containing a Rossmann-like fold.Protein science : a publication of the Protein Society · 2018Article
- Transcriptome guided identification of novel functions of RECQ1 helicase.Methods (San Diego, Calif.) · 2016Article
- Altered RECQ Helicase Expression in Sporadic Primary Colorectal Cancers.Translational oncology · 2013Article
- DNA repair and genome maintenance in Bacillus subtilis.Microbiology and molecular biology reviews : MMBR · 2012Review
- Translocation of E. coli RecQ helicase on single-stranded DNA.Biochemistry · 2012Article
- Beyond Genetics in Glioma Pathways: The Ever-Increasing Crosstalk between Epigenomic and Genomic Events.Journal of signal transduction · 2012Article
- p53 null fluorescent yellow direct repeat (FYDR) mice have normal levels of homologous recombination.DNA repair · 2011Article
- Critical interaction domains between bloom syndrome protein and RAD51.The protein journal · 2011Article
- Recql5 plays an important role in DNA replication and cell survival after camptothecin treatment.Molecular biology of the cell · 2009Article
- Human RECQ1 is a DNA damage responsive protein required for genotoxic stress resistance and suppression of sister chromatid exchanges.PloS one · 2007Article
- RECQL, a member of the RecQ family of DNA helicases, suppresses chromosomal instability.Molecular and cellular biology · 2007Article
- Nascent DNA processing by RecJ favors lesion repair over translesion synthesis at arrested replication forks in Escherichia coli.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Rqh1 blocks recombination between sister chromatids during double strand break repair, independent of its helicase activity.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Redundancy of DNA helicases in p53-mediated apoptosis.Oncogene · 2006Article
- Sit down, relax and unwind: structural insights into RecQ helicase mechanisms.Nucleic acids research · 2006Review
- Examination of the roles of Sgs1 and Srs2 helicases in the enforcement of recombination fidelity in Saccharomyces cerevisiae.Genetics · 2004Article
- Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes.Molecular and cellular biology · 2004Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RecQ family DNA helicases are defined as proteins sharing a homologous region with Escherichia coli RecQ and are basically regarded as enzymes involved in recombination. Humans have five RecQ family members, and deficiencies in three of them, BLM, WRN, and RTS, cause Bloom's, Werner's, and Rothmund-Thomson syndromes, respectively, each characterized by genomic instability and cancer predisposition. In this context, an important function of the RecQ homologs appears to be the unwinding of intermediates of recombination, thereby preventing its uncontrolled execution. As a consequence, their deficiencies give rise to elevated levels of recombination (the hyper-recombination phenotype), which result in chromosomal aberrations including loss of heterozygosity, a common chromosomal change associated with malignancies. Thus, those helicases qualify as caretaker-type tumor suppressor proteins. In addition, BLM and WRN deficiencies have been shown to attenuate p53-mediated apoptosis, suggesting that they also belong to the gatekeeper class of tumor suppressor proteins.
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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.