ArticleStem cell reports2016
Endogenous DNA Damage Leads to p53-Independent Deficits in Replicative Fitness in Fetal Murine Fancd2
Article in Stem cell reports, 2016. 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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Who cites it
8 citing papers in PubMed.
- A porcine model of Fanconi anemia.PloS one · 2025Article
- Deregulated protein homeostasis constrains fetal hematopoietic stem cell pool expansion in Fanconi anemia.Nature communications · 2024Article
- RUNX1 mutations mitigate quiescence to promote transformation of hematopoietic progenitors in Fanconi anemia.Leukemia · 2023Article
- Replication stress increases mitochondrial metabolism and mitophagy in FANCD2 deficient fetal liver hematopoietic stem cells.Frontiers in oncology · 2023Article
- Abnormal migration behavior linked to Rac1 signaling contributes to primordial germ cell exhaustion in Fanconi anemia pathway-deficient Fancg-/- embryos.Human molecular genetics · 2021Article
- An induced pluripotent stem cell model of Fanconi anemia reveals mechanisms of p53-driven progenitor cell differentiation.Blood advances · 2020Article
- Studies in an Early Development Window Unveils a Severe HSC Defect in both Murine and Human Fanconi Anemia.Stem cell reports · 2018Article
- Loss of the homologous recombination geneProceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Our mechanistic understanding of Fanconi anemia (FA) pathway function in hematopoietic stem and progenitor cells (HSPCs) owes much to their role in experimentally induced DNA crosslink lesion repair. In bone marrow HSPCs, unresolved stress confers p53-dependent apoptosis and progressive cell attrition. The role of FA proteins during hematopoietic development, in the face of physiological replicative demand, remains elusive. Here, we reveal a fetal HSPC pool in Fancd2
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Registered trials
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