N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility. - Wikidata - wikimedia - TriplyDB

N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility.

N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility.

http://www.wikidata.org/entity/Q36561910

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Xin proteins and intercalated disc maturation, signaling and diseases Cortactin is required for N-cadherin regulation of Kv1.5 channel function N-cadherin/catenin complex as a master regulator of intercalated disc function Loss of cadherin-binding proteins β-catenin and plakoglobin in the heart leads to gap junction remodeling and arrhythmogenesis Conditional ablation of nonmuscle myosin II-B delineates heart defects in adult mice Cardiac tissue-restricted deletion of plakoglobin results in progressive cardiomyopathy and activation of {beta}-catenin signaling Ordered assembly of the adhesive and electrochemical connections within newly formed intercalated disks in primary cultures of adult rat cardiomyocytes Cadherins as targets for genetic diseases.Effects of cardiac-restricted overexpression of the A(2A) adenosine receptor on adriamycin-induced cardiotoxicity Remodeling of cardiac fibroblasts following myocardial infarction results in increased gap junction intercellular communication Mechanisms of gap junction traffic in health and disease Novel methods of automated quantification of gap junction distribution and interstitial collagen quantity from animal and human atrial tissue sections.Assembly of connexin43 into gap junctions is regulated differentially by E-cadherin and N-cadherin in rat liver epithelial cells.Arrhythmogenic properties of dismantling cadherin-mediated adhesion in murine hearts.Cell junctions in the specialized conduction system of the heart The spatiotemporal development of intercalated disk in three-dimensional engineered heart tissues based on collagen/matrigel matrix On the role of the gap junction protein Cx43 (GJA1) in human cardiac malformations with Fallot-pathology. a study on paediatric cardiac specimen.Connexin43 phosphorylation in brain, cardiac, endothelial and epithelial tissues.The connexin43 carboxyl terminus and cardiac gap junction organization Loss of αT-catenin alters the hybrid adhering junctions in the heart and leads to dilated cardiomyopathy and ventricular arrhythmia following acute ischemia Connexin 43 is an emerging therapeutic target in ischemia/reperfusion injury, cardioprotection and neuroprotection Cell-cell junction remodeling in the heart: possible role in cardiac conduction system function and arrhythmias?Cell-cell connection to cardiac disease New insights into the roles of Xin repeat-containing proteins in cardiac development, function, and disease.Connexin43 phosphorylation: structural changes and biological effects.Cell-cell junctional proteins in cardiovascular mechanotransduction.Gap junctions and arrhythmogenic cardiomyopathy.N-cadherin-mediated adhesion and signaling from development to disease: lessons from mice.Trafficking highways to the intercalated disc: new insights unlocking the specificity of connexin 43 localization.Alterations in cell adhesion proteins and cardiomyopathy.Xin Scaffolding Proteins and Arrhythmias Whole exome sequencing with genomic triangulation implicates CDH2-encoded N-cadherin as a novel pathogenic substrate for arrhythmogenic cardiomyopathy.Rapid Discovery of De Novo Deleterious Mutations in Cattle Enhances the Value of Livestock as Model Species.A change of heart: heterogeneous remodeling in heart failure.Effects of ischemic preconditioning on ischemia/reperfusion-induced arrhythmias by upregulatation of connexin 43 expression.Electrical stimulation directs engineered cardiac tissue to an age-matched native phenotype.Effects of doxycycline on cx43 distribution and cardiac arrhythmia susceptibility of rats after myocardial infarction.Hematopoietic stem cells do not depend on N-cadherin to regulate their maintenance.Comparative effects of torasemide and furosemide on gap junction proteins and cardiac fibrosis in a rat model of dilated cardiomyopathy.Requirement for N-cadherin-catenin complex in heart development.

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P2860

N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility.

http://www.wikidata.org/entity/Q36561910

description

2007 nî lūn-bûn

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2007年の論文

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2007年論文

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2007年論文

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2007年論文

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2007年论文

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2007年论文

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2007年论文

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name

N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

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N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

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N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

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N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

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prefLabel

N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

@ast

N-cadherin haploinsufficiency ...... and arrhythmic susceptibility.

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Journal of Molecular and Cellular Cardiology

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N-cadherin haploinsufficiency affects cardiac gap junctions and arrhythmic susceptibility

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Glenn L Radice

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Jifen Li

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Nataliya Petrenko

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Vickas V Patel

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Yanming Xiong

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P2860

The gap junction protein connexin43 interacts with the second PDZ domain of the zona occludens-1 protein

Involvement of ZO-1 in cadherin-based cell adhesion through its direct binding to alpha catenin and actin filaments

Chronic pressure overload cardiac hypertrophy and failure in guinea pigs: III. Intercalated disc remodeling

Dynamics of early contact formation in cultured adult rat cardiomyocytes studied by N-cadherin fused to green fluorescent protein

Remodeling the intercalated disc leads to cardiomyopathy in mice misexpressing cadherins in the heart

The area composita of adhering junctions connecting heart muscle cells of vertebrates. I. Molecular definition in intercalated disks of cardiomyocytes by immunoelectron microscopy of desmosomal proteins

N-cadherin in adult rat cardiomyocytes in culture. I. Functional role of N-cadherin and impairment of cell-cell contact by a truncated N-cadherin mutant

Induced deletion of the N-cadherin gene in the heart leads to dissolution of the intercalated disc structure

Conduction slowing and sudden arrhythmic death in mice with cardiac-restricted inactivation of connexin43

N-cadherin signals through Rac1 determine the localization of connexin 43 in cardiac myocytes

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18201716

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haploinsufficiency

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