Flow-activated transport events along the nephron
Wang T. Flow-activated transport events along the nephron. Current Opinion In Nephrology & Hypertension 2006, 15: 530-536. PMID: 16914967, DOI: 10.1097/01.mnh.0000242180.46362.c4.Peer-Reviewed Original ResearchConceptsBrush-border microvilliProximal tubulesCultured proximal tubule cellsProximal tubules in vitroGlomerular filtration rateProximal tubule cellsBrush-borderH-ATPase activityTubules in vitroNHE3 activityHCO3- absorptionENOS translocationTubule cellsFiltration rateMg2+ transportReceptor localizationSignal transduction mechanismsH-ATPaseHormonal regulationCa2+NephronTubulesResponse to flowTransduction mechanismsIntact actin cytoskeletonHMG-CoA reductase inhibitor simvastatin mitigates VEGF-induced “inside-out” signaling to extracellular matrix by preventing RhoA activation
Xu H, Zeng L, Peng H, Chen S, Jones J, Chew TL, Sadeghi MM, Kanwar YS, Danesh FR. HMG-CoA reductase inhibitor simvastatin mitigates VEGF-induced “inside-out” signaling to extracellular matrix by preventing RhoA activation. American Journal Of Physiology. Renal Physiology 2006, 291: f995-f1004. PMID: 16774905, DOI: 10.1152/ajprenal.00092.2006.Peer-Reviewed Original ResearchMeSH KeywordsActin CytoskeletonActinsAnimalsCells, CulturedCollagen Type IVExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesHydroxymethylglutaryl-CoA Reductase InhibitorsIntegrin beta1Mesangial CellsMevalonic AcidPhosphorylationProlineRatsrhoA GTP-Binding ProteinSignal TransductionSimvastatinTritiumTyrosineVascular Endothelial Growth Factor AConceptsRhoA activationIntact actin cytoskeletonCell signaling cascadesPrecise signaling mechanismUnderlying molecular mechanismsActin cytoskeletonECM expansionMevalonate depletionSignaling cascadesIntegrin activationMevalonate pathwayECM accumulationMolecular mechanismsVEGF stimulationSignaling mechanismComplex biologyExtracellular matrixPleiotropic effectsAngiogenic polypeptideType IV collagen accumulationEndothelial cell permeabilityExtracellular matrix accumulationCell permeabilityGrowth factorPathological processesStimulation of Gαq-coupled M1 muscarinic receptor causes reversible spectrin redistribution mediated by PLC, PKC and ROCK
Street M, Marsh SJ, Stabach PR, Morrow JS, Brown DA, Buckley NJ. Stimulation of Gαq-coupled M1 muscarinic receptor causes reversible spectrin redistribution mediated by PLC, PKC and ROCK. Journal Of Cell Science 2006, 119: 1528-1536. PMID: 16551696, DOI: 10.1242/jcs.02872.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium-Calmodulin-Dependent Protein KinasesCricetinaeCyclophosphamideDoxorubicinGTP-Binding Protein alpha Subunits, Gq-G11Intracellular Signaling Peptides and ProteinsProtein Kinase CProtein Serine-Threonine KinasesReceptor, Muscarinic M1Receptors, Muscarinicrho-Associated KinasesSignal TransductionSpectrinType C PhospholipasesVincristineConceptsG protein-coupled receptorsAlphaII-spectrinSpecialized plasma membrane domainsPlasma membrane domainsIntact actin cytoskeletonStimulation of GPCRsProtein kinase CExtracellular stimuliActin cytoskeletonProtein complexesM1 muscarinic receptorsMembrane domainsMembrane blebbingPlasma membraneCytoskeletal proteinsKinase ROCKMolecular mechanismsConstitutive activationKinase CCellular localizationGlobal rearrangementsPhospholipase CSpectrinCHO cellsReversible redistribution
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