alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice
about
Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the AtriaCav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilageGenetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathyNovel protective role of endogenous cardiac myocyte P2X4 receptors in heart failureMicrodomain-specific localization of functional ion channels in cardiomyocytes: an emerging concept of local regulation and remodelling.TRPC channels are necessary mediators of pathologic cardiac hypertrophy.Electrophysiological remodeling in heart failurec-kit+ cells minimally contribute cardiomyocytes to the heartThe IP3 receptor regulates cardiac hypertrophy in response to select stimuli.β-Adrenergic stimulation increases Cav3.1 activity in cardiac myocytes through protein kinase APhorbol ester and endothelin-1 alter functional expression of Na+/Ca2+ exchange, K+, and Ca2+ currents in cultured neonatal rat myocytesT-type Ca²+ signalling regulates aldosterone-induced CREB activation and cell death through PP2A activation in neonatal cardiomyocytesRegulation and function of Cav3.1 T-type calcium channels in IGF-I-stimulated pulmonary artery smooth muscle cells.P2X4 receptor-eNOS signaling pathway in cardiac myocytes as a novel protective mechanism in heart failure.Genetic Analysis of Connective Tissue Growth Factor as an Effector of Transforming Growth Factor β Signaling and Cardiac Remodeling.The PTIP-Associated Histone Methyltransferase Complex Prevents Stress-Induced Maladaptive Cardiac Remodeling.Functional brown adipose tissue limits cardiomyocyte injury and adverse remodeling in catecholamine-induced cardiomyopathy.The Mitochondrial Calcium Uniporter Selectively Matches Metabolic Output to Acute Contractile Stress in the HeartCaveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in CardiomyocytesTropomyosin dephosphorylation results in compensated cardiac hypertrophyGenetic lineage tracing identifies in situ Kit-expressing cardiomyocytes.Syndecan 4 signaling is required for exercise-induced cardiac hypertrophy.T-type Ca²⁺ channels regulate the exit of cardiac myocytes from the cell cycle after birth.Adenylyl cyclase 6 deletion increases mortality during sustained β-adrenergic receptor stimulation.CaMKII in the cardiovascular system: sensing redox states.Functional importance of T-type voltage-gated calcium channels in the cardiovascular and renal system: news from the world of knockout mice.Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes.Cytokine Effects on Mechano-Induced Electrical Activity in Atrial Myocardium.T-type Ca2+ channels and autoregulation of local blood flow.Decreased cardiac L-type Ca²⁺ channel activity induces hypertrophy and heart failure in mice.Cardiac-directed expression of a catalytically inactive adenylyl cyclase 6 protects the heart from sustained β-adrenergic stimulation.Molecular pathways underlying cardiac remodeling during pathophysiological stimulation.Ca(2+) influx through L-type Ca(2+) channels and transient receptor potential channels activates pathological hypertrophy signalingA caveolae-targeted L-type Ca²+ channel antagonist inhibits hypertrophic signaling without reducing cardiac contractility.Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.Early growth response 1 is an early signal inducing Cav3.2 T-type calcium channels during cardiac hypertrophy.TNF-α provokes electrical abnormalities in rat atrial myocardium via a NO-dependent mechanism.Evodiamine inhibits angiotensin II-induced rat cardiomyocyte hypertrophy.Increasing T-type calcium channel activity by β-adrenergic stimulation contributes to β-adrenergic regulation of heart rates.P/Q-type and T-type voltage-gated calcium channels are involved in the contraction of mammary and brain blood vessels from hypertensive patients.
P2860
Q28511764-BDB10FE4-8FD1-442D-99F0-29542B386787Q30578389-F8D09AFF-F6A9-4047-BC43-B863A45A0215Q30583137-FC97BBF1-7458-4D78-99B6-71B5FA74CE6EQ30614182-79CB8BB0-0208-4FEE-8CC6-04C1F71033A5Q33659429-6F78A6FB-D4A3-4839-BD94-996C78C2EB90Q33859656-22C7576F-9A65-4572-A6F4-D6CC441872DAQ33887264-AB29FB2A-4E90-42EC-94C4-82C6C69FC982Q34021586-EB603A26-CAB3-4F7C-A351-AA5C33D8DAF8Q34103732-2112BF65-6DA0-4B17-BCA3-6F87728EC6CBQ34341705-A17DEC86-9838-43BA-8E3F-2122071F8342Q34600447-9786C0E6-D143-499D-B230-4DFB8131421DQ34682845-5FDE5502-F1E1-493F-8F4F-646C4C9C7DC9Q34718076-138B1150-A7F2-4F88-A797-8C4688685D56Q35143680-92AAFBC9-B59A-407A-9E44-6B3355AF1E24Q35626083-95B213D7-0311-4E05-857E-52D1DD45397EQ35639445-916E1929-A406-4505-889D-84C64E9435A1Q35751292-F77E3B0A-4960-440E-8B0E-EE98424DFAD1Q35836414-3B108335-C194-4DCA-8597-CD5A4411B5E3Q36065247-7D48780D-9FC9-4588-AD0C-B530C40B1D35Q36492849-3B7C5326-2522-4125-A79B-C95782334AE3Q36751620-FDE3DE98-24F9-406A-A4F0-7403685A009CQ37216988-70450FF3-67C3-428A-9186-33156DBA10FCQ37466162-46B577BD-103D-4A8D-BADA-2EAC26634165Q37704624-E307E28D-49EB-45F7-A864-68019952D589Q37899670-A5869846-8967-4407-83CA-36FF3C65D4BDQ38292292-184BEC06-51C0-427F-A997-8707C5481A64Q38822292-24F0AA27-849A-41F6-A3DE-364EFF2FB41BQ38951853-DC422E84-7D82-44DC-AD47-153A4EAEA0C9Q39068338-684D7667-9E55-44DD-B819-9065086ABFB4Q40053441-55E03882-ABA1-4867-9616-823668828438Q41212496-1F23CCF3-7C5C-4A5A-93EF-6D7756EDFE70Q41855920-DF67A730-889E-47C5-AE37-81B76C994AB9Q42425047-8664B168-A37C-44DB-A8D0-68F04D743450Q42550135-03DA6003-7EDD-4E7A-AD6F-02625B1E5E64Q42592376-24EA886E-38BD-46D1-B93F-7AABA6F3D57AQ43471762-247B1D76-D2C7-4951-A7F9-259928BD6CE2Q44368109-1028139C-5B1D-428C-B66C-8317CE4A8C6BQ47850883-0267DBB8-AB70-4E85-8B4B-D9F7F31CE20DQ48045540-B147334B-9441-4714-A95D-0E97B0ECB9A1Q48690663-63E165D7-318E-41F2-9C21-2245779CF67B
P2860
alpha1G-dependent T-type Ca2+ current antagonizes cardiac hypertrophy through a NOS3-dependent mechanism in mice
description
2009 nî lūn-bûn
@nan
2009年の論文
@ja
2009年論文
@yue
2009年論文
@zh-hant
2009年論文
@zh-hk
2009年論文
@zh-mo
2009年論文
@zh-tw
2009年论文
@wuu
2009年论文
@zh
2009年论文
@zh-cn
name
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@en
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@nl
type
label
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@en
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@nl
prefLabel
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@en
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@nl
P2093
P2860
P356
P1476
alpha1G-dependent T-type Ca2+ ...... S3-dependent mechanism in mice
@en
P2093
Arnold Schwartz
Hiroyuki Nakayama
Ilona Bodi
Jeffrey Robbins
John Lorenz
Robert N Correll
Steven R Houser
P2860
P304
P356
10.1172/JCI39724
P407
P577
2009-11-16T00:00:00Z