ArticleeLife2015
Loss of neurofibromin Ras-GAP activity enhances the formation of cardiac blood islands in murine embryos.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- NF1 and SPRED1/2 cooperate through RAS-MAPK-independent functions.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Zebrafish neurofibromatosis type 1 mutants show disruption of sleep but not of circadian rhythms.Sleep · 2026Article
- Critical role of cell competition in gliomagenesis.bioRxiv : the preprint server for biology · 2026Article
- Generation of heterozygous and homozygous NF1 lines from human-induced pluripotent stem cells using CRISPR/Cas9 to investigate bone defects associated with neurofibromatosis type 1.Frontiers in cell and developmental biology · 2024Article
- Exploring the Molecular Landscape of Myelofibrosis, with a Focus on Ras and Mitogen-Activated Protein (MAP) Kinase Signaling.Cancers · 2023Review
- PDGFRβCell reports · 2022Article
- Case report: multiple gastrointestinal stroma tumors in the background of neurofibromatosis type 1.Journal of surgical case reports · 2020Article
- Pumping the brakes on RAS - negative regulators and death effectors of RAS.Journal of cell science · 2020Review
- Genetic and genomic alterations differentially dictate low-grade glioma growth through cancer stem cell-specific chemokine recruitment of T cells and microglia.Neuro-oncology · 2019Article
- Endothelial to Mesenchymal Transition in Cardiovascular Disease: JACC State-of-the-Art Review.Journal of the American College of Cardiology · 2019Review
- Physiology of Cardiac Development: From Genetics to Signaling to Therapeutic Strategies.Current opinion in physiology · 2018Article
- Alternative Progenitor Cells Compensate to Rebuild the Coronary Vasculature in Elabela- and Apj-Deficient Hearts.Developmental cell · 2017Article
- Emerging genotype-phenotype relationships in patients with large NF1 deletions.Human genetics · 2017Review
- Coronary Artery Development: Progenitor Cells and Differentiation Pathways.Annual review of physiology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Type I neurofibromatosis (NF1) is caused by mutations in the NF1 gene encoding neurofibromin. Neurofibromin exhibits Ras GTPase activating protein (Ras-GAP) activity that is thought to mediate cellular functions relevant to disease phenotypes. Loss of murine Nf1 results in embryonic lethality due to heart defects, while mice with monoallelic loss of function mutations or with tissue-specific inactivation have been used to model NF1. Here, we characterize previously unappreciated phenotypes in Nf1-/- embryos, which are inhibition of hemogenic endothelial specification in the dorsal aorta, enhanced yolk sac hematopoiesis, and exuberant cardiac blood island formation. We show that a missense mutation engineered into the active site of the Ras-GAP domain is sufficient to reproduce ectopic blood island formation, cardiac defects, and overgrowth of neural crest-derived structures seen in Nf1-/-embryos. These findings demonstrate a role for Ras-GAP activity in suppressing the hemogenic potential of the heart and restricting growth of neural crest-derived tissues.
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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.