ArticleCirculation2019
Nexilin Is a New Component of Junctional Membrane Complexes Required for Cardiac T-Tubule Formation.
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 86 citations in OpenAlex.
- Transcriptional readthrough at Atf4 locus suppresses Rps19bp1 and impairs heart development.Cardiovascular research · 2026Article
- Nexilin promotes calcium-dependent endo-lysosomal fission required for retrograde transport.Cell communication and signaling : CCS · 2026Article
- Circulating excitation-contraction coupling proteins and incident cardiovascular outcomes: associations and incremental predictive performance in the UK Biobank.Frontiers in cardiovascular medicine · 2026Article
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- ASNA1 is essential for cardiac development and function by regulating tail-anchored protein stability and vesicular transport in cardiomyocytes.PLoS genetics · 2025Article
- Calcium handling remodeling in dilated cardiomyopathy: From molecular mechanisms to targeted therapies.Channels (Austin, Tex.) · 2025Review
- Right Ventricular Myocardial Strain and Proteomic Analysis of Fetuses With Left Ventricular Hypoplasia: A Cross-Sectional Study.Health science reports · 2025Article
- Transcriptional Readthrough atbioRxiv : the preprint server for biology · 2025Article
- RBPMS and RBPMS2 Cooperate to Safeguard Cardiac Splicing.Circulation research · 2025Article
- Genetic and Phenotypic Characterization of Nexilin (NEXN)-Related Cardiomyopathy: Results From a Multicentric Study.JACC. Heart failure · 2025Article
- NEXN protects against vascular calcification by promoting SERCA2 SUMOylation and stabilization.Nature communications · 2025Article
- NEXN deficiency leads to dilated cardiomyopathy in human pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2025Article
- Deletion ofJournal of developmental biology · 2025Article
- Early Stage Morphogenesis of Transverse Tubules in Rat Cardiomyocytes: The Role of pBIN1.Circulation research · 2025Article
- NEXN regulates vascular smooth muscle cell phenotypic switching and neointimal hyperplasia.JCI insight · 2025Article
- Intronic RNAscope probes enable precise identification of cardiomyocyte nuclei and cell cycle activity.Communications biology · 2025Article
- Nexilin mutations, a cause of chronic heart failure: A state-of-the-art review starting from a clinical case.World journal of cardiology · 2025Review
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Transposition of the Great Arteries With Intact Ventricular Septum and Fetal-Onset Dilated Cardiomyopathy in a Neonate With a Homozygous NEXN Variant.Case reports in pediatrics · 2025Article
- Article
2 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMembrane contact sites are fundamental for transmission and translation of signals in multicellular organisms. The junctional membrane complexes in the cardiac dyads, where transverse (T) tubules are juxtaposed to the sarcoplasmic reticulum, are a prime example. T-tubule uncoupling and remodeling are well-known features of cardiac disease and heart failure. Even subtle alterations in the association between T-tubules and the junctional sarcoplasmic reticulum can cause serious cardiac disorders. NEXN (nexilin) has been identified as an actin-binding protein, and multiple mutations in the NEXN gene are associated with cardiac diseases, but the precise role of NEXN in heart function and disease is still unknown.
methodsNexn global and cardiomyocyte-specific knockout mice were generated. Comprehensive phenotypic and RNA sequencing and mass spectrometry analyses were performed. Heart tissue samples and isolated single cardiomyocytes were analyzed by electron and confocal microscopy.
resultsGlobal and cardiomyocyte-specific loss of Nexn in mice resulted in a rapidly progressive dilated cardiomyopathy. In vivo and in vitro analyses revealed that NEXN interacted with junctional sarcoplasmic reticulum proteins, was essential for optimal calcium transients, and was required for initiation of T-tubule invagination and formation.
conclusionsThese results demonstrated that NEXN is a pivotal component of the junctional membrane complex and is required for initiation and formation of T-tubules, thus providing insight into mechanisms underlying cardiomyopathy in patients with mutations in NEXN.
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