ArticleGenes & development2001
The murine winged helix transcription factors, Foxc1 and Foxc2, are both required for cardiovascular development and somitogenesis.
Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers, 1 of them a synthesis that pooled it.
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Who cites it
154 citing papers in PubMed, 1 synthesis or guideline pooled it, 354 citations in OpenAlex.
- Variable Anterior Segment Dysgenesis and Cardiac Anomalies Caused by a Novel Truncating Variant of FOXC1.Genes · 2022Pooled it
- Article
- Classification of indeterminate and off-target cell types within human kidney organoid differentiation.iScience · 2026Article
- Clinical presentation and genotype-phenotype correlation of a novel pure duplication of 6p25.2-p22.3: a case report and literature review.Molecular cytogenetics · 2026Article
- FOXC1 Controls Smooth Muscle Cell Differentiation and Plasticity in Vascular Disease.JACC. Basic to translational science · 2026Article
- PAX3: A Driver of Normal Development and Disease.Biomolecules · 2026Review
- Gateway analysis reveals transient molecular programs at cell-fate transitions.bioRxiv : the preprint server for biology · 2026Article
- Application of Prenatal Whole Exome Sequencing for Congenital Heart Anomalies.International journal of molecular sciences · 2026Review
- Embryotoxicity analysis of anti-arrhythmia drugs amiodarone, dronedarone, and their metabolites using 3D gastruloid models.Reproductive toxicology (Elmsford, N.Y.) · 2025Article
- Downregulation of serum Foxc2 in dilated cardiomyopathy: association with disease severity and cardiac function.Future science OA · 2025Article
- Detection of developmental toxicity of the anti-COVID-19 drug molnupiravir using gastruloid-based in vitro assays.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- Size-dependent temporal decoupling of morphogenesis and transcriptional programs in pseudoembryos.Science advances · 2025Article
- Foxf1-mediated co-regulation of miR-495 and let-7c modulates epicardial cell migration and myocardial specification.Cellular and molecular life sciences : CMLS · 2025Article
- A spatially organizedScience advances · 2025Article
- FOXC1 and retinopathy: targeting molecular mechanisms in retinal blood vessel growth.Expert opinion on therapeutic targets · 2024Article
- Genome-Wide Expression Profiling and Phenotypic Analysis of Downstream Targets Identify the Fox Transcription Factor Jumeau as a Master Regulator of Cardiac Progenitor Cell Division.International journal of molecular sciences · 2024Article
- NR4A1 and NR4A2 orphan nuclear receptors regulate endothelial-to-hematopoietic transition in mouse hematopoietic stem cell specification.Development (Cambridge, England) · 2024Article
- Pleiotropy in FOXC1-attributable phenotypes involves altered ciliation and cilia-dependent signaling.Scientific reports · 2024Article
- FOXC1 and FOXC2 regulate growth plate chondrocyte maturation towards hypertrophy in the embryonic mouse limb skeleton.Development (Cambridge, England) · 2024Article
- Functional FOXC1 variants in familial and sporadic atrial septal defect with cellular and animal validation.Clinical and translational medicine · 2024Article
94 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The murine Foxc1/Mf1 and Foxc2/Mfh1 genes encode closely related forkhead/winged helix transcription factors with overlapping expression in the forming somites and head mesoderm and endothelial and mesenchymal cells of the developing heart and blood vessels. Embryos lacking either Foxc1 or Foxc2, and most compound heterozygotes, die pre- or perinatally with similar abnormal phenotypes, including defects in the axial skeleton and cardiovascular system. However, somites and major blood vessels do form. This suggested that the genes have similar, dose-dependent functions, and compensate for each other in the early development of the heart, blood vessels, and somites. In support of this hypothesis, we show here that compound Foxc1; Foxc2 homozygotes die earlier and with much more severe defects than single homozygotes alone. Significantly, they have profound abnormalities in the first and second branchial arches, and the early remodeling of blood vessels. Moreover, they show a complete absence of segmented paraxial mesoderm, including anterior somites. Analysis of compound homozygotes shows that Foxc1 and Foxc2 are both required for transcription in the anterior presomitic mesoderm of paraxis, Mesp1, Mesp2, Hes5, and Notch1, and for the formation of sharp boundaries of Dll1, Lfng, and ephrinB2 expression. We propose that the two genes interact with the Notch signaling pathway and are required for the prepatterning of anterior and posterior domains in the presumptive somites through a putative Notch/Delta/Mesp regulatory loop.
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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.