TRPV2 is critical for the maintenance of cardiac structure and function in mice. - Test2 - elhamkhani - TriplyDB

TRPV2 is critical for the maintenance of cardiac structure and function in mice.

TRPV2 is critical for the maintenance of cardiac structure and function in mice.

http://www.wikidata.org/entity/Q33729367

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TRPV1: A Target for Rational Drug Design Cryo-electron microscopy structure of the TRPV2 ion channel Engineering vanilloid-sensitivity into the rat TRPV2 channel Role of TRP channels in the cardiovascular system.The transient receptor potential vanilloid 2 cation channel is abundant in macrophages accumulating at the peri-infarct zone and may enhance their migration capacity towards injured cardiomyocytes following myocardial infarction Transient Receptor Potential Vanilloid 2 Regulates Myocardial Response to Exercise Quantifying Drug-Induced Nanomechanics and Mechanical Effects to Single Cardiomyocytes for Optimal Drug Administration To Minimize Cardiotoxicity.The Akt-mTOR axis is a pivotal regulator of eccentric hypertrophy during volume overload.TRPV2 knockout mice demonstrate an improved cardiac performance following myocardial infarction due to attenuated activity of peri-infarct macrophages.Lack of TRPV2 impairs thermogenesis in mouse brown adipose tissue Axial stretch-dependent cation entry in dystrophic cardiomyopathy: Involvement of several TRPs channels Protective effects of intercalated disk protein afadin on chronic pressure overload-induced myocardial damage.The role of transient receptor potential channels in hypertension and metabolic vascular damage.Functional TRPV2 and TRPV4 channels in human cardiac c-kit(+) progenitor cells.Fam64a is a novel cell cycle promoter of hypoxic fetal cardiomyocytes in mice.Predictive model identifies key network regulators of cardiomyocyte mechano-signaling.Probenecid Improves Cardiac Function in Patients With Heart Failure With Reduced Ejection Fraction In Vivo and Cardiomyocyte Calcium Sensitivity In Vitro.Induced NCX1 overexpression attenuates pressure overload-induced pathological cardiac remodelling.Novel inhibitor candidates of TRPV2 prevent damage of dystrophic myocytes and ameliorate against dilated cardiomyopathy in a hamster model.The role of transient receptor potential vanilloid 2 channel in cardiac aging.Dystrophic cardiomyopathy: role of TRPV2 channels in stretch-induced cell damage.A TRPV2 interactome-based signature for prognosis in glioblastoma patients.MECHANOMEDICINE: applications of mechanobiology to medical sciences and next-generation medical technologies TRPV2 is required for mechanical nociception and the stretch-evoked response of primary sensory neurons

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

http://www.wikidata.org/entity/Q33729367

description

2014 nî lūn-bûn

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2014 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2014 թվականի մայիսին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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name

TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

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Nature Communications

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TRPV2 is critical for the maintenance of cardiac structure and function in mice.

@en

P2093

Atsushi Sudo

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Keiichiro Iwasaki

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Keiji Naruse

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Kimiaki Katanosaka

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Koki Nishitsuji

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Motoi Kanagawa

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Satomi Takatsu

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Satoshi Mohri

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Tatsushi Toda

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Yoshihiro Ujihara

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P2860

Activity-dependent IGF-1 exocytosis is controlled by the Ca(2+)-sensor synaptotagmin-10

Matrix elasticity directs stem cell lineage specification

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

A recessive mutation in desmoplakin causes arrhythmogenic right ventricular dysplasia, skin disorder, and woolly hair

Dilated cardiomyopathy: a disease of the intercalated disc?

Ultrastructural evidence of intercalated disc remodelling in arrhythmogenic right ventricular cardiomyopathy: an electron microscopy investigation on endomyocardial biopsies

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

Translocation of a calcium-permeable cation channel induced by insulin-like growth factor-I

Loss of PI3Kγ enhances cAMP-dependent MMP remodeling of the myocardial N-cadherin adhesion complexes and extracellular matrix in response to early biomechanical stress

Cooperative coupling of cell-matrix and cell-cell adhesions in cardiac muscle

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10.1038/NCOMMS4932

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5

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1028306696

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