The non-homologous end-joining activity is required for Fanconi anemia fetal HSC maintenance

摘要

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.