ArticleAmerican journal of physiology. Heart and circulatory physiology2007
Loss of mXinalpha, an intercalated disk protein, results in cardiac hypertrophy and cardiomyopathy with conduction defects.
Article in American journal of physiology. Heart and circulatory physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 70 citations in OpenAlex.
- Fractionated proteomics identifies a protein network mitigating resistance exercise-induced damage in human skeletal muscle.Nature communications · 2026Article
- Single-cell and spatial transcriptomics of the infarcted heart define the dynamic onset of the border zone in response to mechanical destabilization.Nature cardiovascular research · 2022Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice.Journal of visualized experiments : JoVE · 2021Article
- Effects of CMYA1 overexpression on cardiac structure and function in mice.Acta biochimica et biophysica Sinica · 2021Article
- Intercalated disc protein Xinβ is required for Hippo-YAP signaling in the heart.Nature communications · 2020Article
- Critical Roles of Xirp Proteins in Cardiac Conduction and Their Rare Variants Identified in Sudden Unexplained Nocturnal Death Syndrome and Brugada Syndrome in Chinese Han Population.Journal of the American Heart Association · 2018Article
- When signalling goes wrong: pathogenic variants in structural and signalling proteins causing cardiomyopathies.Journal of muscle research and cell motility · 2017Review
- Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017Review
- Myozap Deficiency Promotes Adverse Cardiac Remodeling via Differential Regulation of Mitogen-activated Protein Kinase/Serum-response Factor and β-Catenin/GSK-3β Protein Signaling.The Journal of biological chemistry · 2016Article
- Cell junctions in the specialized conduction system of the heart.Cell communication & adhesion · 2014Review
- Alterations in cell adhesion proteins and cardiomyopathy.World journal of cardiology · 2014Review
- The role of vertebrate nonmuscle Myosin II in development and human disease.Bioarchitecture · 2014Review
- New insights into the roles of Xin repeat-containing proteins in cardiac development, function, and disease.International review of cell and molecular biology · 2014Review
- Quantitative phosphoproteomic study of pressure-overloaded mouse heart reveals dynamin-related protein 1 as a modulator of cardiac hypertrophy.Molecular & cellular proteomics : MCP · 2013Article
- Xin Scaffolding Proteins and Arrhythmias.Journal of cardiology & clinical research · 2013Article
- Identification of Xin-repeat proteins as novel ligands of the SH3 domains of nebulin and nebulette and analysis of their interaction during myofibril formation and remodeling.Molecular biology of the cell · 2013Article
- Intercalated disc protein, mXinα, suppresses p120-catenin-induced branching phenotype via its interactions with p120-catenin and cortactin.Archives of biochemistry and biophysics · 2013Article
- Localization and function of Xinα in mouse skeletal muscle.American journal of physiology. Cell physiology · 2013Article
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11 authors at 1 institution in 1 country.
Funding
Abstract
The intercalated disk protein Xin was originally discovered in chicken striated muscle and implicated in cardiac morphogenesis. In the mouse, there are two homologous genes, mXinalpha and mXinbeta. The human homolog of mXinalpha, Cmya1, maps to chromosomal region 3p21.2-21.3, near a dilated cardiomyopathy with conduction defect-2 locus. Here we report that mXinalpha-null mouse hearts are hypertrophied and exhibit fibrosis, indicative of cardiomyopathy. A significant upregulation of mXinbeta likely provides partial compensation and accounts for the viability of the mXinalpha-null mice. Ultrastructural studies of mXinalpha-null mouse hearts reveal intercalated disk disruption and myofilament disarray. In mXinalpha-null mice, there is a significant decrease in the expression level of p120-catenin, beta-catenin, N-cadherin, and desmoplakin, which could compromise the integrity of the intercalated disks and functionally weaken adhesion, leading to cardiac defects. Additionally, altered localization and decreased expression of connexin 43 are observed in the mXinalpha-null mouse heart, which, together with previously observed abnormal electrophysiological properties of mXinalpha-deficient mouse ventricular myocytes, could potentially lead to conduction defects. Indeed, ECG recordings on isolated, perfused hearts (Langendorff preparations) show a significantly prolonged QT interval in mXinalpha-deficient hearts. Thus mXinalpha functions in regulating the hypertrophic response and maintaining the structural integrity of the intercalated disk in normal mice, likely through its association with adherens junctional components and actin cytoskeleton. The mXinalpha-knockout mouse line provides a novel model of cardiac hypertrophy and cardiomyopathy with conduction defects.
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