2020
Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt
Baratta VM, Norz V, Barahona MJ, Gisinger TM, Mulligan D, Geibel JP. Penicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt. Cellular Physiology And Biochemistry 2020, 54: 1132-1142. PMID: 33175479, PMCID: PMC8095381, DOI: 10.33594/000000305.Peer-Reviewed Original ResearchConceptsRat colonic cryptsColonic cryptsNitric oxideNitric oxide-dependent mechanismPotassium homeostasisArginine methyl esterAmmonium prepulse techniqueIntracellular nitric oxideSodium-free conditionsL-NAMEDiarrheal statesATPase activityBACKGROUND/Presence of NOPenicillin G sodium saltAcute exposureL-arginineSmall intestineIsolated administrationN-nitroHomeostatic conditionsCryptsPrepulse techniqueSignificant reductionNovel mechanism
2014
The Putative Role of the Non-Gastric H+/K+-ATPase ATP12A (ATP1AL1) as Anti-Apoptotic Ion Transporter: Effect of the H+/K+ ATPase Inhibitor SCH28080 on Butyrate-Stimulated Myelomonocytic HL-60 Cells
Jakab M, Hofer S, Ravasio A, Huber F, Schmidt S, Hitzl W, Geibel JP, Fürst J, Ritter M. The Putative Role of the Non-Gastric H+/K+-ATPase ATP12A (ATP1AL1) as Anti-Apoptotic Ion Transporter: Effect of the H+/K+ ATPase Inhibitor SCH28080 on Butyrate-Stimulated Myelomonocytic HL-60 Cells. Cellular Physiology And Biochemistry 2014, 34: 1507-1526. PMID: 25322912, DOI: 10.1159/000366355.Peer-Reviewed Original ResearchConceptsIntracellular acid loadHL-60 cellsAcute intracellular acid loadAcid loadMCV measurementsOsmotic cell shrinkageReal-time reverse transcription PCREarly apoptosisChanges of intracellularCD86 expressionFlow cytometric determinationReverse transcription-PCRBACKGROUND/Intracellular acidosisLoss of intracellularCell shrinkageHigher MCVFlow cytometryRT-PCRATP12APhosphatidylserine exposureUntreated cellsPotential roleMCVApoptosis