ArticleMolecular and cellular biology2012
14-3-3ε plays a role in cardiac ventricular compaction by regulating the cardiomyocyte cell cycle.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- Significance of 14-3-3 Epsilon for Right Ventricular Failure Associated with Pulmonary Hypertension.Internal medicine (Tokyo, Japan) · 2026Article
- 14-3-3 proteins: Regulators of cardiac excitation-contraction coupling and stress responses.The Journal of physiology · 2026Review
- 14-3-3ε: a protein with complex physiology function but promising therapeutic potential in cancer.Cell communication and signaling : CCS · 2024Review
- The dispensability of 14-3-3 proteins for the regulation of human cardiac sodium channel Nav1.5.PloS one · 2024Article
- Is 14-3-3 the Combination to Unlock New Pathways to Improve Metabolic Homeostasis and β-Cell Function?Diabetes · 2023Review
- Altered contractility, CaAmerican journal of physiology. Heart and circulatory physiology · 2023Article
- Polycomb Group Protein CBX7 Represses Cardiomyocyte Proliferation Through Modulation of the TARDBP/RBM38 Axis.Circulation · 2023Article
- 14-3-3 protein regulation of excitation-contraction coupling.Pflugers Archiv : European journal of physiology · 2022Review
- The interaction protein of SORBS2 in myocardial tissue to find out the pathogenic mechanism of LVNC disease.Aging · 2022Article
- Case Report: First Case of Non-restrictive Ventricular Septal Defect With Congestive Heart Failure in a Chinese Han Male Infant Carrying a Class II Chromosome 17p13.3 Microduplication.Frontiers in pediatrics · 2022Article
- The Multifaceted Therapeutic Mechanisms of Curcumin in Osteosarcoma: State-of-the-Art.Journal of oncology · 2021Review
- Article
- Possible key microRNAs and corresponding molecular mechanisms for atrial fibrillation.Anatolian journal of cardiology · 2020Article
- Extensive Changes in Transcriptomic "Fingerprints" and Immunological Cells in the Large Organs of Patients Dying of Acute Septic Shock and Multiple Organ Failure Caused byFrontiers in cellular and infection microbiology · 2020Article
- Semi-automatic detection of myocardial trabeculation using cardiovascular magnetic resonance: correlation with histology and reproducibility in a mouse model of non-compaction.Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance · 2018Article
- Maternal Proteins That Are Phosphoregulated upon Egg Activation Include Crucial Factors for Oogenesis, Egg Activation and Embryogenesis inG3 (Bethesda, Md.) · 2018Article
- Potential Common Pathogenic Pathways for the Left Ventricular Noncompaction Cardiomyopathy (LVNC).Pediatric cardiology · 2018Article
- Neddylation mediates ventricular chamber maturation through repression of Hippo signaling.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- 14-3-3ε is a nuclear matrix protein, and its altered expression and localization are associated with curcumin-induced apoptosis of MG-63 cells.Oncology letters · 2018Article
- Inherited Cardiomyopathies and the Role of Mutations in Non-coding Regions of the Genome.Frontiers in cardiovascular medicine · 2018Review
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
Trabecular myocardium accounts for the majority of the ventricles during early cardiogenesis, but compact myocardium is the primary component at later developmental stages. Elucidation of the genes regulating compact myocardium development is essential to increase our understanding of left ventricular noncompaction (LVNC), a cardiomyopathy characterized by increased ratios of trabecular to compact myocardium. 14-3-3ε is an adapter protein expressed in the lateral plate mesoderm, but its in vivo cardiac functions remain to be defined. Here we show that 14-3-3ε is expressed in the developing mouse heart as well as in cardiomyocytes. 14-3-3ε deletion did not appear to induce compensation by other 14-3-3 isoforms but led to ventricular noncompaction, with features similar to LVNC, resulting from a selective reduction in compact myocardium thickness. Abnormal compaction derived from a 50% decrease in cardiac proliferation as a result of a reduced number of cardiomyocytes in G(2)/M and the accumulation of cardiomyocytes in the G(0)/G(1) phase of the cell cycle. These defects originated from downregulation of cyclin E1 and upregulation of p27(Kip1), possibly through both transcriptional and posttranslational mechanisms. Our work shows that 14-3-3ε regulates cardiogenesis and growth of the compact ventricular myocardium by modulating the cardiomyocyte cell cycle via both cyclin E1 and p27(Kip1). These data are consistent with the long-held view that human LVNC may result from compaction arrest, and they implicate 14-3-3ε as a new candidate gene in congenital human cardiomyopathies.
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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.