2010
Ethanol Inhibits Gastric Acid Secretion in Rats Through Increased AMP-Kinase Activity
Kopic S, Corradini S, Sidani S, Murek M, Vardanyan A, Föller M, Ritter M, Geibel JP. Ethanol Inhibits Gastric Acid Secretion in Rats Through Increased AMP-Kinase Activity. Cellular Physiology And Biochemistry 2010, 25: 195-202. PMID: 20110680, DOI: 10.1159/000276553.Peer-Reviewed Original ResearchConceptsGastric acid secretionAcid secretionSecretagogue-induced acid secretionInhibits gastric acid secretionShort-term ethanol exposurePH-sensitive dye BCECFLow-dose ethanolCompound CAMPK inhibitor compound CSpecific AMPK inhibitor compound CEffects of ethanolInhibitor compound CEthanol exposureRat gastric glandsActivation of AMPKInteraction of ethanolRat gastric parietal cellsFluorescence digital imagingGastric parietal cellsAMP kinase activityDye BCECFInhibitory effectSecretionParietal cellsAMPK pathway
2007
Ethanol inhibits gastric acid secretion in rats through increased AMP‐K activity
Corradini S, Kopic S, Ritter M, Geibel J. Ethanol inhibits gastric acid secretion in rats through increased AMP‐K activity. The FASEB Journal 2007, 21: a1317-a1317. DOI: 10.1096/fasebj.21.6.a1317-c.Peer-Reviewed Original ResearchSecretagogue-induced acid secretionAcid secretionRate of alkalinizationLow-dose ethanol exposureCompound CPH-sensitive dye BCECFLow-dose ethanolGastric acid secretionInhibitor compound CEthanol exposureRat gastric glandsVariety of cellsNH4Cl prepulseRat gastric parietal cellsGastric parietal cellsSecretagogue carbacholPotent modulatorDye BCECFInhibitory effectParietal cellsSecretionGastric glandsAMP kinasePresent studyGland
2006
Hypertonic Saline Attenuates Colonic Tumor Cell Metastatic Potential by Activating Transmembrane Sodium Conductance
Shields CJ, Winter DC, Geibel JP, O’Sullivan G, Wang JH, Redmond HP. Hypertonic Saline Attenuates Colonic Tumor Cell Metastatic Potential by Activating Transmembrane Sodium Conductance. The Journal Of Membrane Biology 2006, 211: 35-42. PMID: 16988862, DOI: 10.1007/s00232-006-0011-8.Peer-Reviewed Original ResearchConceptsHypertonic salineSodium-hydrogen exchangeIntegrin expressionIntracellular sodiumMetastatic potentialHuman colonic tumor cellsAdhesion molecule expressionSodium concentrationColonic tumor cellsTumor cell metastatic potentialIntracellular pHCell metastatic potentialCytosolic sodium concentrationMolecule expressionΒ1 integrin expressionHyperosmolar solutionsConfocal laser microscopic imagingEffect of hypertonicityTumor cellsInhibitory effectSodium responseHypertonic exposureCellular alkalinizationTumor cell-endothelial interactionsSodium conductance
2004
Inhibition of NHE-1 Na+/H+ exchanger by natriuretic peptides in ocular nonpigmented ciliary epithelium
Fidzinski P, Salvador-Silva M, Choritz L, Geibel J, Coca-Prados M. Inhibition of NHE-1 Na+/H+ exchanger by natriuretic peptides in ocular nonpigmented ciliary epithelium. American Journal Of Physiology - Cell Physiology 2004, 287: c655-c663. PMID: 15140751, DOI: 10.1152/ajpcell.00552.2003.Peer-Reviewed Original ResearchConceptsC-type natriuretic peptideAtrial natriuretic peptideBrain natriuretic peptideNatriuretic peptideIntraocular pressureCiliary epitheliumNHE activityNatriuretic peptides atrial natriuretic peptideInhibitory effectType B receptorsNHE-1 activityNonpigmented ciliary epitheliumCell layerGap junction blockersDose-dependent mannerInhibitors of NHEOcular ciliary epitheliumRate of intracellularHypotensive effectJunction blockersTrabecular meshworkMammalian eyeExchanger activityB receptorNHE-1
2001
Effects of the Serine/Threonine Kinase SGK1 on the Epithelial Na+ Channel (ENaC) and CFTR: Implications for Cystic Fibrosis
Wagner C, Ott M, Klingel K, Beck S, Melzig J, Friedrich B, Wild K, Bröer S, Moschen I, Albers A, Waldegger S, Tümmler B, Egan M, Geibel J, Kandolf R, Lang F. Effects of the Serine/Threonine Kinase SGK1 on the Epithelial Na+ Channel (ENaC) and CFTR: Implications for Cystic Fibrosis. Cellular Physiology And Biochemistry 2001, 11: 209-218. PMID: 11509829, DOI: 10.1159/000051935.Peer-Reviewed Original ResearchMeSH Keywords1-Methyl-3-isobutylxanthineAmino Acid SubstitutionAnimalsBronchiCell LineCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorEpithelial CellsEpithelial Sodium ChannelsHumansIn Situ HybridizationLungMacrophages, AlveolarMutationOocytesPatch-Clamp TechniquesProtein Serine-Threonine KinasesPulmonary AlveoliRNA, ComplementaryRNA, MessengerSodiumSodium ChannelsXenopus laevisConceptsSerine/threonine kinase SGK1Lung tissueCystic fibrosisCF patientsKinase SGK1CF lung tissueXenopus oocytesLoss of CFTRLung epithelial cell lineCoexpression of CFTREffect of SGK1Pathophysiological factorsEpithelial cell lineRespiratory epitheliumLung phenotypeVariety of stimuliCl(-) secretionSGK1 expressionInhibitor amilorideInhibitory effectEpithelial cellsEnhanced expressionChannel ENaC.CFTR mutationsChannel activity
1993
Mechanism of apical K+ channel modulation in principal renal tubule cells. Effect of inhibition of basolateral Na(+)-K(+)-ATPase.
Wang W, Geibel J, Giebisch G. Mechanism of apical K+ channel modulation in principal renal tubule cells. Effect of inhibition of basolateral Na(+)-K(+)-ATPase. The Journal Of General Physiology 1993, 101: 673-694. PMID: 8393065, PMCID: PMC2216783, DOI: 10.1085/jgp.101.5.673.Peer-Reviewed Original ResearchConceptsEffect of inhibitionPump inhibitionInhibitory effectChannel activityProtein kinase CPump activityAddition of strophanthidinPatch-clamp techniqueRenal tubule cellsBath solutionCell-attached patchesExtracellular Ca2Removal of Ca2Intracellular Ca2MicroM ionomycinTubule cellsControl valuesLow-conductance K channelsPrincipal cellsChannel modulationK channelsInhibitionNM staurosporineDependent protein kinase CPotent inhibitor