ArticleNucleic acids research2022
RBFOX2 is required for establishing RNA regulatory networks essential for heart development.
Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- PRMT1-SFPQ regulates intron retention to control matrix gene expression during craniofacial development.eLife · 2026Article
- scASprofiler: profiling single-cell RNA splicing with a deep convolutional generative network.Briefings in bioinformatics · 2026Article
- Animal models of hypoplastic left heart syndrome: genetic and anatomical approaches.Pediatric research · 2026Review
- Long non-coding RNA H19 transported by colorectal cancer small extracellular vesicles promotes alternative splicing in healthy hepatocytes: new insights on liver pre-metastatic niche formation.Cell communication and signaling : CCS · 2026Article
- RBFOX2-dependent alternative splicing of Numb regulates Notch signaling during muscle stem cell activation.Stem cell reports · 2026Article
- Alternative splicing dynamics during human cardiac development in vivo and in vitro.Stem cell reports · 2026Article
- Rebalancing NTRK2 isoforms promotes vascular regeneration in bronchopulmonary dysplasia.Cell stem cell · 2026Article
- ExploringCirculation. Genomic and precision medicine · 2025Article
- mExperimental & molecular medicine · 2025Review
- Isoform-Specific Roles of NTRK2 in Pulmonary Vascular Regeneration.bioRxiv : the preprint server for biology · 2025Article
- RBFOX2 induces osteogenic differentiation by Jph2 expression in MC3T3-E1 preosteoblast cells.Molecular biology reports · 2025Article
- RNA-binding protein SAMD4A targets FGF2 to regulate cardiomyocyte lineage specification from human embryonic stem cells.Stem cell research & therapy · 2025Article
- Alternative splicing factors and cardiac disease: more than just missplicing?RNA (New York, N.Y.) · 2025Article
- RNA binding protein with multiple splicing (RBPMS) promotes contractile phenotype splicing in human embryonic stem cell-derived vascular smooth muscle cells.Cardiovascular research · 2024Article
- Alternative Splicing in the Heart: The Therapeutic Potential of Regulating the Regulators.International journal of molecular sciences · 2024Review
- Molecular convergence of risk variants for congenital heart defects leveraging a regulatory map of the human fetal heart.medRxiv : the preprint server for health sciences · 2024Article
- Spontaneously Corrected Hypoplastic Left Heart: A Case Report and Exceptional Opportunity to Discuss Etiology with Novel Therapeutic Vision.Archives of Iranian medicine · 2024Article
- The Biological Mechanisms and Clinical Roles of RNA-Binding Proteins in Cardiovascular Diseases.Biomolecules · 2024Review
- RNA-binding proteins in cardiovascular biology and disease: the beat goes on.Nature reviews. Cardiology · 2024Review
- RNA-Binding Proteins in Cardiomyopathies.Journal of cardiovascular development and disease · 2024Review
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Human genetic studies identified a strong association between loss of function mutations in RBFOX2 and hypoplastic left heart syndrome (HLHS). There are currently no Rbfox2 mouse models that recapitulate HLHS. Therefore, it is still unknown how RBFOX2 as an RNA binding protein contributes to heart development. To address this, we conditionally deleted Rbfox2 in embryonic mouse hearts and found profound defects in cardiac chamber and yolk sac vasculature formation. Importantly, our Rbfox2 conditional knockout mouse model recapitulated several molecular and phenotypic features of HLHS. To determine the molecular drivers of these cardiac defects, we performed RNA-sequencing in Rbfox2 mutant hearts and identified dysregulated alternative splicing (AS) networks that affect cell adhesion to extracellular matrix (ECM) mediated by Rho GTPases. We identified two Rho GTPase cycling genes as targets of RBFOX2. Modulating AS of these two genes using antisense oligos led to cell cycle and cell-ECM adhesion defects. Consistently, Rbfox2 mutant hearts displayed cell cycle defects and inability to undergo endocardial-mesenchymal transition, processes dependent on cell-ECM adhesion and that are seen in HLHS. Overall, our work not only revealed that loss of Rbfox2 leads to heart development defects resembling HLHS, but also identified RBFOX2-regulated AS networks that influence cell-ECM communication vital for heart development.
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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.