ArticleStem cell research & therapy2019
The non-homologous end-joining activity is required for Fanconi anemia fetal HSC maintenance.
Article in Stem cell research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- DNA phenotyping and mapping intragenic deletion mutations in Fanconi anemia: Patterns and diagnostic inferences.Journal, genetic engineering & biotechnology · 2024Article
- Article
- Fanconi anemia: current insights regarding epidemiology, cancer, and DNA repair.Human genetics · 2022Review
- Disabling the Fanconi Anemia Pathway in Stem Cells Leads to Radioresistance and Genomic Instability.Cancer research · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundRecent studies have shown that deficiency in the Fanconi anemia (FA) DNA repair pathway enhances the error-prone non-homologous end-joining (NHEJ) repair, leading to increased genomic instability, and that genetic or pharmacological inhibition of the NHEJ pathway could rescue the FA phenotype.
methodsFirst, we exposed LSK cells from WT and Fanca
resultsInhibition of NHEJ sensitizes HSPCs from Fanca
conclusionThese results demonstrate that the NHEJ pathway functions to maintain Fanconi anemia fetal HSCs.
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