2008
ATP8B1 Deficiency Disrupts the Bile Canalicular Membrane Bilayer Structure in Hepatocytes, But FXR Expression and Activity Are Maintained
Cai S, Gautam S, Nguyen T, Soroka CJ, Rahner C, Boyer JL. ATP8B1 Deficiency Disrupts the Bile Canalicular Membrane Bilayer Structure in Hepatocytes, But FXR Expression and Activity Are Maintained. Gastroenterology 2008, 136: 1060-1069.e4. PMID: 19027009, PMCID: PMC3439851, DOI: 10.1053/j.gastro.2008.10.025.Peer-Reviewed Original ResearchMeSH Keywords4-Chloro-7-nitrobenzofurazanAdenosine TriphosphatasesAnimalsATP Binding Cassette Transporter, Subfamily B, Member 11ATP-Binding Cassette TransportersBile CanaliculiCaco-2 CellsChenodeoxycholic AcidDNA-Binding ProteinsGastrointestinal AgentsGene ExpressionHepatocytesHumansMultidrug Resistance-Associated Protein 2PhosphatidylserinesPhospholipid Transfer ProteinsRatsReceptors, Cytoplasmic and NuclearRNA, Small InterferingTranscription FactorsTransfectionConceptsAminophospholipid flippaseMessenger RNAMembrane bilayer structureCanalicular membraneFarnesoid X receptorRat hepatocytesSmall heterodimer partnerMembrane transportersNBD-phosphatidylserineHeterodimer partnerDeficiency disruptsLuminal accumulationMembrane disruptionRNAConflicting hypothesesRat cellsFlippaseProtein levelsProtein expressionX receptorExpressionBSEP functionATP8B1CellsMembrane
1991
Role of chloride ions in liver cell volume regulation
Haddad P, Beck J, Boyer J, Graf J. Role of chloride ions in liver cell volume regulation. American Journal Of Physiology 1991, 261: g340-g348. PMID: 1872402, DOI: 10.1152/ajpgi.1991.261.2.g340.Peer-Reviewed Original ResearchConceptsRegulatory volume decreaseM omegaLiver cellsSingle isolated rat hepatocytesBiphasic responseHypotonic stressInitial hyperpolarizationPl/minIsolated rat hepatocytesGradual depolarizationCell volume regulationExternal ClRole of C1Hypotonic swellingVolume regulationMembrane potentialFacilitated releaseRat hepatocytesCellsMinVolume decreaseCell volumeInitial volumeInitial rateLiver
1989
Inward-rectifying potassium channels in rat hepatocytes
Henderson R, Graf J, Boyer J. Inward-rectifying potassium channels in rat hepatocytes. American Journal Of Physiology 1989, 256: g1028-g1035. PMID: 2735409, DOI: 10.1152/ajpgi.1989.256.6.g1028.Peer-Reviewed Original ResearchConceptsRenal epithelial cellsRat hepatocytesWhole-cell conductanceWhole-cell experimentsSingle-channel recordingsEpithelial cellsPotassium channelsHigh intracellularFunctional heterogeneityOpen probabilityIsolated rat hepatocytesCellsWhole-cell modeInward rectificationMarked similarityStrong inward rectificationCell conductanceHepatocytesConductanceCalcium dependencePatch-clamp techniqueCurrent-voltage relationshipInward conductanceSpeciesCell experiments
1984
Isolated rat hepatocyte couplets: a primary secretory unit for electrophysiologic studies of bile secretory function.
Graf J, Gautam A, Boyer J. Isolated rat hepatocyte couplets: a primary secretory unit for electrophysiologic studies of bile secretory function. Proceedings Of The National Academy Of Sciences Of The United States Of America 1984, 81: 6516-6520. PMID: 6149546, PMCID: PMC391955, DOI: 10.1073/pnas.81.20.6516.Peer-Reviewed Original ResearchConceptsBile secretory functionElectrophysiologic studySecretory functionHepatocyte coupletsOrganic anion fluoresceinSteady-state intracellularCanalicular lumenCanalicular vacuoleInput resistanceRat liverCollagenase perfusionIntact liverLiverSecretionParacellular barrierBile canalicular lumenSecretory unitsLumenCellsJunctional pathwayElectrical driving forcePerfusion
1974
Ultrastructural changes in livers of two patients with hypervitaminosis A.
Hruban Z, Russell R, Boyer J, Glagov S, Bagheri S. Ultrastructural changes in livers of two patients with hypervitaminosis A. American Journal Of Pathology 1974, 76: 451-61. PMID: 4416771, PMCID: PMC1910880.Peer-Reviewed Original ResearchConceptsPerisinusoidal fibrosisDistinctive ultrastructural changesChronic hypervitaminosis ALipid-storing cellsUltrastructural changesHypervitaminosis AHypervitaminosis A.Blood flowCellular atrophyFibrosisIto cellsMesenchymal cellsPatientsBasement membraneLiverMassive accumulationCellsNumerous bundlesAtrophyLymphocytesBullaeImpairment