ArticlePLoS genetics2022
TGFβ pathway is required for viable gestation of Fanconi anemia embryos.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- miR-29a-3p and TGF-β Axis in Fanconi anemia: mechanisms driving metabolic dysfunction and genome stability.Cellular and molecular life sciences : CMLS · 2025Article
- Integrated multiomic analysis identifies TRIP13 as a mediator of alveolar epithelial type II cell dysfunction in idiopathic pulmonary fibrosis.Biochimica et biophysica acta. Molecular basis of disease · 2025Article
- Deregulated protein homeostasis constrains fetal hematopoietic stem cell pool expansion in Fanconi anemia.Nature communications · 2024Article
- SARS-CoV-2 Spike Protein Induces Oxidative Stress and Senescence in Mouse and Human Lung.In vivo (Athens, Greece)Article
- Chemical Carcinogen (3-Methylcholanthrene)-induced Pleomorphic Rhabdomyosarcomas in Fanconi Anemia Fancd2-/-, Fancg-/- (C57BL/6), Fancd2-/- (129/Sv) Mice.In vivo (Athens, Greece)Article
- Chemical Carcinogen (Dimethyl-benzanthracene) Induced Transplantable Cancer in Fanconi Anemia (Fanca-/-) Mice.In vivo (Athens, Greece)Article
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Overexpression of the TGFβ pathway impairs the proliferation of the hematopoietic stem and progenitor cells (HSPCs) pool in Fanconi anemia (FA). TGFβ promotes the expression of NHEJ genes, known to function in a low-fidelity DNA repair pathway, and pharmacological inhibition of TGFβ signaling rescues FA HSPCs. Here, we demonstrate that genetic disruption of Smad3, a transducer of the canonical TGFβ pathway, modifies the phenotype of FA mouse models deficient for Fancd2. We observed that the TGFβ and NHEJ pathway genes are overexpressed during the embryogenesis of Fancd2-/- mice and that the Fancd2-/-Smad3-/- double knockout (DKO) mice undergo high levels of embryonic lethality due to loss of the TGFβ-NHEJ axis. Fancd2-deficient embryos acquire extensive genomic instability during gestation which is not reversed by Smad3 inactivation. Strikingly, the few DKO survivors have activated the non-canonical TGFβ-ERK pathway, ensuring expression of NHEJ genes during embryogenesis and improved survival. Activation of the TGFβ-NHEJ axis was critical for the survival of the few Fancd2-/-Smad3-/- DKO newborn mice but had detrimental consequences for these surviving mice, such as enhanced genomic instability and ineffective hematopoiesis.
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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.