ArticleJournal of molecular medicine (Berlin, Germany)2016
NFAT5-mediated CACNA1C expression is critical for cardiac electrophysiological development and maturation.
Article in Journal of molecular medicine (Berlin, Germany), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Gene expression regulation by CaCellular & molecular biology letters · 2026Pooled it
- CALHM5 deficiency alleviates aortic aneurysm by regulating smooth muscle calcium homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Calcium channel-coupled transcription factors facilitate direct nuclear signaling.Research square · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- A Review of theDiseases (Basel, Switzerland) · 2024Review
- LncRNA Gm43843 Promotes Cardiac Hypertrophy via miR-153-3p/Cacna1c Axis.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- NFAT5-Mediated Signalling Pathways in Viral Infection and Cardiovascular Dysfunction.International journal of molecular sciences · 2021Review
- Assessment of temporal functional changes and miRNA profiling of human iPSC-derived cardiomyocytes.Scientific reports · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledEntry of calcium into cardiomyocyte via L-type calcium channel (LTCC) is fundamental to cardiac contraction. CACNA1C, a type of LTCC and a hallmark of a matured ventricular myocyte, is developmentally regulated. Here, we identified 138 potential transcription factors by a comparative genomic study on 5-kb promoter regions of CACNA1C gene across eight vertebrate species, and showed that six factors were developmentally regulated with the expression of Cacna1c in mouse P19cl6 in vitro cardiomyocyte differentiation model. We further demonstrated that the nuclear factor of activated T cells 5 (Nfat5) bound to a consensus sequence TGGAAGCGTTC and activated the transcription of Cacna1c. The siRNA-mediated knockdown of Nfat5 suppressed the expression of Cacna1c and decreased L-type calcium current in mouse neonatal cardiomyocytes. Furthermore, morpholino-mediated knockdown of nfat5 in zebrafish prohibited the expression of cacna1c and resulted in a non-contractile ventricle, while over-expression of either cacna1c or nfat5 rescued this impaired phenotype. Thus, NFAT5-mediated expression of CACNA1C is evolutionarily conserved and critical for cardiac electrophysiological development and maturation of cardiomyocyte. KEY MESSAGE: Nfat5 binds to a consensus sequence TGGAAGCGTTC in the promoter of Cacna1c. Nfat5 activates the transcription of Cacna1c. Nfat5 knockdown suppresses Cacna1c expression, decreases L-type calcium current, and results in non-beating ventricle. NFAT5-mediated expression of CACNA1C is evolutionarily conserved. NFAT5-mediated CACNA1C expression is critical for cardiac electrophysiological development and maturation.
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Registered trials
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