ArticleOncogene2006
Redundancy of DNA helicases in p53-mediated apoptosis.
Article in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 26 citations in OpenAlex.
- Polydopamine Nanoparticle-Based Combined Chemotherapy and Photothermal Therapy for the Treatment of Liver Cancer.ACS applied materials & interfaces · 2024Article
- Review
- Article
- Expression microarray identifies the unliganded glucocorticoid receptor as a regulator of gene expression in mammary epithelial cells.BMC cancer · 2014Article
- On BLM helicase in recombination-mediated telomere maintenance.Molecular biology reports · 2013Article
- RecQ helicases; at the crossroad of genome replication, repair, and recombination.Molecular biology reports · 2012Review
- RECQL5 cooperates with Topoisomerase II alpha in DNA decatenation and cell cycle progression.Nucleic acids research · 2012Article
- Telomere attrition and genomic instability in xeroderma pigmentosum type-b deficient fibroblasts under oxidative stress.Journal of cellular and molecular medicine · 2010Article
- Genomic instability resulting from Blm deficiency compromises development, maintenance, and function of the B cell lineage.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Depletion of WRN enhances DNA damage in HeLa cells exposed to the benzene metabolite, hydroquinone.Mutation research · 2008Article
- Model of human aging: recent findings on Werner's and Hutchinson-Gilford progeria syndromes.Clinical interventions in aging · 2008Review
- Other proteins interacting with XP proteins.Advances in experimental medicine and biology · 2008Review
- Murine Pif1 interacts with telomerase and is dispensable for telomere function in vivo.Molecular and cellular biology · 2007Article
- Mechanisms of RecQ helicases in pathways of DNA metabolism and maintenance of genomic stability.The Biochemical journal · 2006Review
- Epigenetic inactivation of the premature aging Werner syndrome gene in human cancer.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
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 3 institutions in 2 countries.
Funding
Abstract
A subset of DNA helicases, the RecQ family, has been found to be associated with the p53-mediated apoptotic pathway and is involved in maintaining genomic integrity. This family contains the BLM and WRN helicases, in which germline mutations are responsible for Bloom and Werner syndromes, respectively. TFIIH DNA helicases, XPB and XPD, are also components in this apoptotic pathway. We hypothesized that there may be some redundancy between helicases in their ability to complement the attenuated p53-mediated apoptotic levels seen in cells from individuals with diseases associated with these defective helicase genes. The attenuated apoptotic phenotype in Bloom syndrome cells was rescued not only by ectopic expression of BLM, but also by WRN or XPB, both 3' --> 5' helicases, but not expression of the 5' --> 3' helicase XPD. Overexpression of Sgs1, a WRN/BLM yeast homolog, corrected the reduction in BS cells only, which is consistent with Sgs1 being evolutionarily most homologous to BLM. A restoration of apoptotic levels in cells from WS, XPB or XPD patients was attained only by overexpression of the specific helicase. Our data suggest a limited redundancy in the pathways of these RecQ helicases in p53-induced apoptosis.
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.