Endothelin-1-stimulated InsP3-induced Ca2+ release is a nexus for hypertrophic signaling in cardiac myocytes. - Wikidata - awgldk - TriplyDB

Endothelin-1-stimulated InsP3-induced Ca2+ release is a nexus for hypertrophic signaling in cardiac myocytes.

Endothelin-1-stimulated InsP3-induced Ca2+ release is a nexus for hypertrophic signaling in cardiac myocytes.

http://www.wikidata.org/entity/Q34954184

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Increased InsP3Rs in the junctional sarcoplasmic reticulum augment Ca2+ transients and arrhythmias associated with cardiac hypertrophy Endothelin-1 induces myofibrillar disarray and contractile vector variability in hypertrophic cardiomyopathy-induced pluripotent stem cell-derived cardiomyocytes Phospholipase C epsilon scaffolds to muscle-specific A kinase anchoring protein (mAKAPbeta) and integrates multiple hypertrophic stimuli in cardiac myocytes Phospholipase Cε hydrolyzes perinuclear phosphatidylinositol 4-phosphate to regulate cardiac hypertrophy Location matters: clarifying the concept of nuclear and cytosolic CaMKII subtypes Mutual antagonism between IP(3)RII and miRNA-133a regulates calcium signals and cardiac hypertrophy Nuclear proton dynamics and interactions with calcium signaling Calmodulin binding proteins provide domains of local Ca2+ signaling in cardiac myocytes Phosphorylation of TRPC6 channels at Thr69 is required for anti-hypertrophic effects of phosphodiesterase 5 inhibition Isoform- and tissue-specific regulation of the Ca(2+)-sensitive transcription factor NFAT in cardiac myocytes and heart failure.Inhibition of miR-25 improves cardiac contractility in the failing heart.Rough endoplasmic reticulum to junctional sarcoplasmic reticulum trafficking of calsequestrin in adult cardiomyocytes.The IP3 receptor regulates cardiac hypertrophy in response to select stimuli.Activation of NFATc1 is directly mediated by IP3 in adult cardiac myocytes Role of inositol 1,4,5-trisphosphate in the regulation of ventricular Ca(2+) signaling in intact mouse heart.Nuclear calcium is required for human T cell activation.Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes.Selective activation of the transcription factor NFAT1 by calcium microdomains near Ca2+ release-activated Ca2+ (CRAC) channels.Succinate causes pathological cardiomyocyte hypertrophy through GPR91 activation.Endoplasmic reticulum Ca(2+) handling in excitable cells in health and disease Stimulus-dependent regulation of nuclear Ca2+ signaling in cardiomyocytes: a role of neuronal calcium sensor-1.Protein kinase D3 is a pivotal activator of pathological cardiac hypertrophy by selectively increasing the expression of hypertrophic transcription factors.The type 2 inositol 1,4,5-trisphosphate receptor, emerging functions for an intriguing Ca²⁺-release channel.Cardiomyocyte Antihypertrophic Effect of Adipose Tissue Conditioned Medium from Rats and Its Abrogation by Obesity is Mediated by the Leptin to Adiponectin Ratio.Calsequestrin accumulation in rough endoplasmic reticulum promotes perinuclear Ca2+ release Emerin plays a crucial role in nuclear invagination and in the nuclear calcium transient The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth.Alzheimer's disease-associated peptide Aβ42 mobilizes ER Ca(2+) via InsP3R-dependent and -independent mechanisms.The H3K9 dimethyltransferases EHMT1/2 protect against pathological cardiac hypertrophy Calcineurin-NFATc regulates type 2 inositol 1,4,5-trisphosphate receptor (InsP3R2) expression during cardiac remodeling.Nuclear membrane receptors for ET-1 in cardiovascular function.Role of the nuclear envelope in calcium signalling.An integrated mechanism of cardiomyocyte nuclear Ca(2+) signaling.Insights from human congenital disorders of intestinal lipid metabolism.Regulation of phosphatidylinositol-specific phospholipase C at the nuclear envelope in cardiac myocytes.Vitamin D: a custodian of cell signalling stability in health and disease.Tropisetron inhibits high glucose-induced calcineurin/NFAT hypertrophic pathway in H9c2 myocardial cells.Vitamin D, reactive oxygen species and calcium signalling in ageing and disease.Cardiac inositol 1,4,5-trisphosphate receptors.Increases in intracellular sodium activate transcription and gene expression via the salt-inducible kinase 1 network in an atrial myocyte cell line.

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P2860

Endothelin-1-stimulated InsP3-induced Ca2+ release is a nexus for hypertrophic signaling in cardiac myocytes.

http://www.wikidata.org/entity/Q34954184

description

2009 nî lūn-bûn

@nan

2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի փետրվարին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

@zh-hk

2009年論文

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2009年論文

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2009年论文

@wuu

name

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@ast

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@en

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@nl

type

label

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@ast

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@en

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@nl

prefLabel

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@ast

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@en

Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes.

@nl

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J.MOLCEL.2009.02.005

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Endothelin-1-stimulated InsP3- ...... signaling in cardiac myocytes

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Amarnath Talasila

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Claire J Fearnley

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Daniel R Higazi

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Elaine M Corps

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Faye M Drawnel

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Fraser McDonald

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33

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H Llewelyn Roderick

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24145503

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