ArticleCell cycle (Georgetown, Tex.)2017
Persistent response of Fanconi anemia haematopoietic stem and progenitor cells to oxidative stress.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 13 citations in OpenAlex.
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Estimating the risk of anemia associated with PMCommunications medicine · 2026Article
- Recurrent Constellations of Embryonic Malformations (RCEM): Teratogenicity Linked to Transient Hypoxia and Hormone Pregnancy Tests Agrees With RCEM and Suggest a Reactive Oxygen Species Pathogenesis.Birth defects research · 2026Review
- New Insights into the Fanconi Anemia Pathogenesis: A Crosstalk Between Inflammation and Oxidative Stress.International journal of molecular sciences · 2024Review
- Article
- Upregulation of NKG2D ligands impairs hematopoietic stem cell function in Fanconi anemia.The Journal of clinical investigation · 2022Article
- MRE11-dependent instability in mitochondrial DNA fork protection activates a cGAS immune signaling pathway.Science advances · 2021Article
- Direct and Indirect Effects of Indoor Particulate Matter on Blood Indicators Related to Anemia.International journal of environmental research and public health · 2021Article
- MYC Promotes Bone Marrow Stem Cell Dysfunction in Fanconi Anemia.Cell stem cell · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Oxidative stress is considered as an important pathogenic factor in many human diseases including Fanconi anemia (FA), an inherited bone marrow failure syndrome with extremely high risk of leukemic transformation. Members of the FA protein family are involved in DNA damage and other cellular stress responses. Loss of FA proteins renders cells hypersensitive to oxidative stress and cancer transformation. However, how FA cells respond to oxidative DNA damage remains unclear. By using an in vivo stress-response mouse strain expressing the Gadd45β-luciferase transgene, we show here that haematopoietic stem and progenitor cells (HSPCs) from mice deficient for the FA gene Fanca or Fancc persistently responded to oxidative stress. Mechanistically, we demonstrated that accumulation of unrepaired DNA damage, particularly in oxidative damage-sensitive genes, was responsible for the long-lasting response in FA HSPCs. Furthermore, genetic correction of Fanca deficiency almost completely abolished the persistent oxidative stress-induced G
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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.