ArticleProceedings of the National Academy of Sciences of the United States of America2018
Interaction between cardiac myosin-binding protein C and formin Fhod3.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- The formin Fhod3 is required for sarcomere reassembly after mitosis in postnatal cardiomyocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Mavacamten shows broad benefit in human and mouse models of MYBPC3-related hypertrophic cardiomyopathy.Nature cardiovascular research · 2026Article
- Human formin FHOD3-mediated actin elongation is required for sarcomere integrity in cardiomyocytes.eLife · 2025Article
- The expression of the formin Fhod3 in mouse tongue striated muscle.Cell structure and function · 2024Article
- Bringing into focus the central domains C3-C6 of myosin binding protein C.Frontiers in physiology · 2024Review
- Article
- Advanced searching for hypertrophic cardiomyopathy heritability in real practice tomorrow.Frontiers in cardiovascular medicine · 2023Review
- FHODs: Nuclear tethered formins for nuclear mechanotransduction.Frontiers in cell and developmental biology · 2023Review
- The Mechanisms of Thin Filament Assembly and Length Regulation in Muscles.International journal of molecular sciences · 2022Review
- Whole genome sequencing delineates regulatory, copy number, and cryptic splice variants in early onset cardiomyopathy.NPJ genomic medicine · 2022Article
- Minor hypertrophic cardiomyopathy genes, major insights into the genetics of cardiomyopathies.Nature reviews. Cardiology · 2022Review
- Genome-wide association study of cardiac troponin I in the general population.Human molecular genetics · 2021Article
- Variant Spectrum of Formin Homology 2 Domain-Containing 3 Gene in Chinese Patients With Hypertrophic Cardiomyopathy.Journal of the American Heart Association · 2021Article
- Myosin Binding Protein-C Forms Amyloid-Like Aggregates In Vitro.International journal of molecular sciences · 2021Article
- Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.Journal of molecular and cellular cardiology · 2020Review
- MyBP-C: one protein to govern them all.Journal of muscle research and cell motility · 2020Review
- Assembly and Maintenance of Sarcomere Thin Filaments and Associated Diseases.International journal of molecular sciences · 2020Review
- Formin homology 2 domain-containing 3 (Fhod3) controls neural plate morphogenesis in mouse cranial neurulation by regulating multidirectional apical constriction.The Journal of biological chemistry · 2019Article
- Skeletal myosin binding protein-C: An increasingly important regulator of striated muscle physiology.Archives of biochemistry and biophysics · 2018Review
- Actin-associated proteins and cardiomyopathy-the 'unknown' beyond troponin and tropomyosin.Biophysical reviews · 2018Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in cardiac myosin-binding protein C (cMyBP-C) are a major cause of familial hypertrophic cardiomyopathy. Although cMyBP-C has been considered to regulate the cardiac function via cross-bridge arrangement at the C-zone of the myosin-containing A-band, the mechanism by which cMyBP-C functions remains unclear. We identified formin Fhod3, an actin organizer essential for the formation and maintenance of cardiac sarcomeres, as a cMyBP-C-binding protein. The cardiac-specific N-terminal Ig-like domain of cMyBP-C directly interacts with the cardiac-specific N-terminal region of Fhod3. The interaction seems to direct the localization of Fhod3 to the C-zone, since a noncardiac Fhod3 variant lacking the cMyBP-C-binding region failed to localize to the C-zone. Conversely, the cardiac variant of Fhod3 failed to localize to the C-zone in the cMyBP-C-null mice, which display a phenotype of hypertrophic cardiomyopathy. The cardiomyopathic phenotype of cMyBP-C-null mice was further exacerbated by Fhod3 overexpression with a defect of sarcomere integrity, whereas that was partially ameliorated by a reduction in the Fhod3 protein levels, suggesting that Fhod3 has a deleterious effect on cardiac function under cMyBP-C-null conditions where Fhod3 is aberrantly mislocalized. Together, these findings suggest the possibility that Fhod3 contributes to the pathogenesis of cMyBP-C-related cardiomyopathy and that Fhod3 is critically involved in cMyBP-C-mediated regulation of cardiac function via direct interaction.
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