Nitric oxide-cGMP-protein kinase G pathway negatively regulates vascular transient receptor potential channel TRPC6. - Test2 - elhamkhani - TriplyDB

Nitric oxide-cGMP-protein kinase G pathway negatively regulates vascular transient receptor potential channel TRPC6.

Nitric oxide-cGMP-protein kinase G pathway negatively regulates vascular transient receptor potential channel TRPC6.

http://www.wikidata.org/entity/Q39962813

about

SNF8, a member of the ESCRT-II complex, interacts with TRPC6 and enhances its channel activity TRP-ing up heart and vessels: canonical transient receptor potential channels and cardiovascular disease Metabolomic profiling of cellular responses to carvedilol enantiomers in vascular smooth muscle cells Complex interactions of NO/cGMP/PKG systems on Ca2+ signaling in afferent arteriolar vascular smooth muscle.Cyclic GMP/PKG-dependent inhibition of TRPC6 channel activity and expression negatively regulates cardiomyocyte NFAT activation Novel mechanism of cardiac stress modulation by PDE5 inhibition Phosphodiesterase 5 inhibition ameliorates angiontensin II-induced podocyte dysmotility via the protein kinase G-mediated downregulation of TRPC6 activity.Phosphorylation of TRPC6 channels at Thr69 is required for anti-hypertrophic effects of phosphodiesterase 5 inhibition Roles of cGMP-dependent protein kinase I (cGKI) and PDE5 in the regulation of Ang II-induced cardiac hypertrophy and fibrosis.cGMP-dependent protein kinases and cGMP phosphodiesterases in nitric oxide and cGMP action.Role of reactive oxygen species and redox in regulating the function of transient receptor potential channels.Membrane potential and Ca2+ concentration dependence on pressure and vasoactive agents in arterial smooth muscle: A model.Endothelial actions of atrial and B-type natriuretic peptides Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters Gain-of-function mutations in transient receptor potential C6 (TRPC6) activate extracellular signal-regulated kinases 1/2 (ERK1/2)Old dog, new tricks: novel cardiac targets and stress regulation by protein kinase G.Sodium tanshinone IIA sulfonate inhibits hypoxia-induced enhancement of SOCE in pulmonary arterial smooth muscle cells via the PKG-PPAR-γ signaling axis The role of cGMP/cGKI signalling and Trpc channels in regulation of vascular tone.Inhibition of TRPC1/TRPC3 by PKG contributes to NO-mediated vasorelaxation.Sildenafil inhibits hypoxia-induced transient receptor potential canonical protein expression in pulmonary arterial smooth muscle via cGMP-PKG-PPARγ axis Hyperactive adverse mechanical stress responses in dystrophic heart are coupled to transient receptor potential canonical 6 and blocked by cGMP-protein kinase G modulation.Regulation of cardiovascular TRP channel functions along the NO-cGMP-PKG axis.TRP channels: sensors and transducers of gasotransmitter signals.Canonical Transient Receptor Potential Channels and Their Link with Cardio/Cerebro-Vascular Diseases.Nitric oxide lacks direct effect on TRPC5 channels but suppresses endogenous TRPC5-containing channels in endothelial cells.TRPC channels function independently of STIM1 and Orai1.Inhibition of SOC/Ca2+/NFAT pathway is involved in the anti-proliferative effect of sildenafil on pulmonary artery smooth muscle cells.Protein kinase C-dependent phosphorylation of transient receptor potential canonical 6 (TRPC6) on serine 448 causes channel inhibition.TRPC3 Channels in Cardiac Fibrosis.Heparin responses in vascular smooth muscle cells involve cGMP-dependent protein kinase (PKG)cAMP activates TRPC6 channels via the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB)-mitogen-activated protein kinase kinase (MEK)-ERK1/2 signaling pathway.The serine 814 of TRPC6 is phosphorylated under unstimulated conditions.Regulation of vascular tone homeostasis by NO and H2S: Implications in hypertension.The Janus-faced regulation of endothelial permeability by cyclic GMP.Protection of Nrf2 against arsenite-induced oxidative damage is regulated by the cyclic guanosine monophosphate-protein kinase G signaling pathway.The regulation of transient receptor potential canonical 4 (TRPC4) channel by phosphodiesterase 5 inhibitor via the cyclic guanosine 3'5'-monophosphate.Lung endothelial Ca2+ and permeability response to platelet-activating factor is mediated by acid sphingomyelinase and transient receptor potential classical 6.Murine cardiac growth, TRPC channels, and cGMP kinase I.Molecular determinants for cardiovascular TRPC6 channel regulation by Ca2+/calmodulin-dependent kinase II.

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Nitric oxide-cGMP-protein kinase G pathway negatively regulates vascular transient receptor potential channel TRPC6.

http://www.wikidata.org/entity/Q39962813

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Nitric oxide-cGMP-protein kina ...... eptor potential channel TRPC6.

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Nitric oxide-cGMP-protein kina ...... eptor potential channel TRPC6.

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Nitric oxide-cGMP-protein kina ...... eptor potential channel TRPC6.

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JPHYSIOL.2008.156083

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The Journal of Physiology

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Nitric oxide-cGMP-protein kina ...... eptor potential channel TRPC6.

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Akira Honda

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Hai Lin

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Masayuki X Mori

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Naomi Geshi

http://www.w3.org/2001/XMLSchema#string

Noboru Takami

http://www.w3.org/2001/XMLSchema#string

Ryuji Inoue

http://www.w3.org/2001/XMLSchema#string

Shinichi Takahashi

http://www.w3.org/2001/XMLSchema#string

Yasuhiro Kawarabayashi

http://www.w3.org/2001/XMLSchema#string

Yasuo Mori

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P2860

Regulation of TRPC6 channel activity by tyrosine phosphorylation

An introduction to TRP channels

The transient receptor potential protein homologue TRP6 is the essential component of vascular alpha(1)-adrenoceptor-activated Ca(2+)-permeable cation channel.

Toward transcriptional therapies for the failing heart: chemical screens to modulate genes

Secretory protein trafficking and organelle dynamics in living cells.

Invited review: cGMP-dependent protein kinase signaling mechanisms in smooth muscle: from the regulation of tone to gene expression.

Ion channels in smooth muscle: regulators of intracellular calcium and contractility.

ER transport signals and trafficking of potassium channels and receptors.

cGMP and S-nitrosylation: two routes for modulation of neuronal excitability by NO.

Calcium, calmodulin, and calcium-calmodulin kinase II: heartbeat to heartbeat and beyond.

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