Activation of NFATc3 Down-regulates the β1 Subunit of Large Conductance, Calcium-activated K+Channels in Arterial Smooth Muscle and Contributes to Hypertension
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Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle DisordersIon channel remodeling in vascular smooth muscle during hypertension: Implications for novel therapeutic approachesInhibition of nuclear factor of activated T-cells (NFAT) suppresses accelerated atherosclerosis in diabetic miceRole of serine-threonine phosphoprotein phosphatases in smooth muscle contractilityNFATc3 mediates chronic hypoxia-induced pulmonary arterial remodeling with alpha-actin up-regulationCerebrovascular dilation via selective targeting of the cholane steroid-recognition site in the BK channel β1-subunit by a novel nonsteroidal agentNuclear factor of activated T cells regulates osteopontin expression in arterial smooth muscle in response to diabetes-induced hyperglycemia.Elevated Ca2+ sparklet activity during acute hyperglycemia and diabetes in cerebral arterial smooth muscle cells.Regulation of large conductance Ca2+-activated K+ (BK) channel β1 subunit expression by muscle RING finger protein 1 in diabetic vessels.Natural inequalities: why some L-type Ca2+ channels work harder than othersThe regulation of BK channel activity by pre- and post-translational modifications.NFATc3 contributes to intermittent hypoxia-induced arterial remodeling in miceRegulation of GPCR signaling in hypertension.Nerve growth factor (NGF) regulates activity of nuclear factor of activated T-cells (NFAT) in neurons via the phosphatidylinositol 3-kinase (PI3K)-Akt-glycogen synthase kinase 3β (GSK3β) pathwayBK channels and a new form of hypertension.Endothelin-1 contributes to increased NFATc3 activation by chronic hypoxia in pulmonary arteries.Selective down-regulation of KV2.1 function contributes to enhanced arterial tone during diabetesNFATc3 is required for chronic hypoxia-induced pulmonary hypertension in adult and neonatal miceTranscriptional responses to intermittent hypoxiaCalcium/calmodulin-dependent kinase II inhibition in smooth muscle reduces angiotensin II-induced hypertension by controlling aortic remodeling and baroreceptor function.NFATc3 and VIP in Idiopathic Pulmonary Fibrosis and Chronic Obstructive Pulmonary DiseaseDistinct activation properties of the nuclear factor of activated T-cells (NFAT) isoforms NFATc3 and NFATc4 in neurons.Creating order from chaos: cellular regulation by kinase anchoring.The β1-subunit of the MaxiK channel associates with the thromboxane A2 receptor and reduces thromboxane A2 functional effectsBK Channels in Cardiovascular Diseases and AgingCapturing single L-type Ca(2+) channel function with opticsLocal regulation of L-type Ca²⁺ channel sparklets in arterial smooth muscleReduced vascular smooth muscle BK channel current underlies heart failure-induced vasoconstriction in mice.NFATc3 regulates BK channel function in murine urinary bladder smooth muscle.The control of Ca2+ influx and NFATc3 signaling in arterial smooth muscle during hypertension.CaV1.2 sparklets in heart and vascular smooth muscleAKAP150 participates in calcineurin/NFAT activation during the down-regulation of voltage-gated K(+) currents in ventricular myocytes following myocardial infarction.Regulation of soluble guanylyl cyclase-alpha1 expression in chronic hypoxia-induced pulmonary hypertension: role of NFATc3 and HuR.Different Effects of Hypertension and Age on the Function of Large Conductance Calcium- and Voltage-Activated Potassium Channels in Human Mesentery Artery Smooth Muscle Cells.Impaired function of coronary BK(Ca) channels in metabolic syndromeIntermittent hypoxia-induced increases in reactive oxygen species activate NFATc3 increasing endothelin-1 vasoconstrictor reactivity.Molecular and biophysical mechanisms of Ca2+ sparklets in smooth muscleMechanisms of intermittent hypoxia induced hypertension.Ser1928 phosphorylation by PKA stimulates the L-type Ca2+ channel CaV1.2 and vasoconstriction during acute hyperglycemia and diabetes.AKAP150 contributes to enhanced vascular tone by facilitating large-conductance Ca2+-activated K+ channel remodeling in hyperglycemia and diabetes mellitus.
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Activation of NFATc3 Down-regulates the β1 Subunit of Large Conductance, Calcium-activated K+Channels in Arterial Smooth Muscle and Contributes to Hypertension
description
article publié dans la revue scientifique Journal of Biological Chemistry
@fr
im Dezember 2006 veröffentlichter wissenschaftlicher Artikel
@de
scientific article published in Journal of Biological Chemistry
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wetenschappelijk artikel
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наукова стаття, опублікована в грудні 2006
@uk
name
Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
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Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
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type
label
Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
@en
Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
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prefLabel
Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
@en
Activation of NFATc3 Down-regu ...... nd Contributes to Hypertension
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P50
P356
P1476
Activation of NFATc3 down-regu ...... nd contributes to hypertension
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P2093
C Blake Nichols
Madeline Nieves-Cintrón
P304
P356
10.1074/JBC.M608822200
P407
P577
2006-12-05T00:00:00Z