ArticleDNA repair2010
Divergent cellular phenotypes of human and mouse cells lacking the Werner syndrome RecQ helicase.
Article in DNA repair, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Detection of nuclear STING in cultured human cells and in the normal and cancer tissues.iScience · 2026Article
- Werner syndrome exonuclease promotes gut regeneration and causes age-associated gut hyperplasia in Drosophila.PLoS biology · 2025Article
- Application of the microfluidic-assisted replication track analysis to measure DNA repair in human and mouse cells.Methods (San Diego, Calif.) · 2016Article
- Regulation of gene expression by the BLM helicase correlates with the presence of G-quadruplex DNA motifs.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Distinct functions of human RECQ helicases WRN and BLM in replication fork recovery and progression after hydroxyurea-induced stalling.DNA repair · 2013Article
- FGFR2 mutation confers a less drastic gain of function in mesenchymal stem cells than in fibroblasts.Stem cell reviews and reports · 2012Article
- Mutator suppression and escape from replication error-induced extinction in yeast.PLoS genetics · 2011Article
- Uracil-DNA glycosylase in base excision repair and adaptive immunity: species differences between man and mouse.The Journal of biological chemistry · 2011Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Werner syndrome (WS) is a human autosomal recessive genetic instability and cancer predisposition syndrome with features of premature aging. Several genetically determined mouse models of WS have been generated, however, none develops features of premature aging or an elevated risk of neoplasia unless additional genetic perturbations are introduced. In order to determine whether differences in cellular phenotype could explain the discrepant phenotypes of Wrn-/- mice and WRN-deficient humans, we compared the cellular phenotype of newly derived Wrn-/- mouse primary fibroblasts with previous analyses of primary and transformed fibroblasts from WS patients and with newly derived, WRN-depleted human primary fibroblasts. These analyses confirmed previously reported cellular phenotypes of WRN-mutant and WRN-deficient human fibroblasts, and demonstrated that the human WRN-deficient cellular phenotype can be detected in cells grown in 5% or in 20% oxygen. In contrast, we did not identify prominent cellular phenotypes present in WRN-deficient human cells in Wrn-/- mouse fibroblasts. Our results indicate that human and mouse fibroblasts have different functional requirements for WRN protein, and that the absence of a strong cellular phenotype may in part explain the failure of Wrn-/- mice to develop an organismal phenotype resembling Werner syndrome.
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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.