2006
The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase
Kovacikova J, Winter C, Loffing-Cueni D, Loffing J, Finberg K, Lifton R, Hummler E, Rossier B, Wagner C. The connecting tubule is the main site of the furosemide-induced urinary acidification by the vacuolar H+-ATPase. Kidney International 2006, 70: 1706-1716. PMID: 16985514, DOI: 10.1038/sj.ki.5001851.Peer-Reviewed Original ResearchMeSH KeywordsAcid-Base EquilibriumAmilorideAnimalsDiureticsEpithelial Sodium ChannelsFurosemideGene Expression RegulationGene Expression Regulation, EnzymologicHydrochlorothiazideHydrogen-Ion ConcentrationKidney Tubules, CollectingKidney Tubules, DistalMetabolic Clearance RateMiceMice, KnockoutNephronsProton-Translocating ATPasesWater-Electrolyte BalanceConceptsUrinary acidificationRenal clearance experimentsEffect of furosemideNormal urinary acidificationLumen-negative voltageNet acid excretionThick ascending limbFinal urinary acidificationKidney-specific inactivationENaC channelsClearance experimentsAcid excretionMouse modelAscending limbFurosemideDuct cellsProton secretionMiceExact localizationReabsorptionMain siteB1 subunitAlpha subunitTubulesFunctional expression
2005
The B1-subunit of the H+ ATPase is required for maximal urinary acidification
Finberg KE, Wagner CA, Bailey MA, Păunescu T, Breton S, Brown D, Giebisch G, Geibel JP, Lifton RP. The B1-subunit of the H+ ATPase is required for maximal urinary acidification. Proceedings Of The National Academy Of Sciences Of The United States Of America 2005, 102: 13616-13621. PMID: 16174750, PMCID: PMC1224669, DOI: 10.1073/pnas.0506769102.Peer-Reviewed Original ResearchConceptsMaximal urinary acidificationNormal urinary acidificationMetabolic acidosisUrinary acidificationDistal renal tubular acidosisAcid challengeRenal tubular acidosisAcute intracellular acidificationB1 subunitLumen-negative potentialFurosemide infusionTubular acidosisAlkaline urineDistal nephronGreater severityAcidosisMiceLoss of B1Intracellular acidificationApical expressionUrineDuctFurther decreaseIsoformsPlasma membrane
1999
Localization of a Gene for Autosomal Recessive Distal Renal Tubular Acidosis with Normal Hearing ( rdRTA2 ) to 7q33-34
Karet F, Finberg K, Nayir A, Bakkaloglu A, Ozen S, Hulton S, Sanjad S, Al-Sabban E, Medina J, Lifton R. Localization of a Gene for Autosomal Recessive Distal Renal Tubular Acidosis with Normal Hearing ( rdRTA2 ) to 7q33-34. American Journal Of Human Genetics 1999, 65: 1656-1665. PMID: 10577919, PMCID: PMC1288376, DOI: 10.1086/302679.Peer-Reviewed Original ResearchMeSH KeywordsAcidosis, Renal TubularAdenosine TriphosphatasesAdultAnion Transport ProteinsAntiportersChildChild, PreschoolChromosome MappingChromosomes, Human, Pair 2Chromosomes, Human, Pair 7ConsanguinityDNA Mutational AnalysisFemaleGenes, RecessiveHearingHumansHydrogen-Ion ConcentrationInfantInfant, NewbornLod ScoreMaleMembrane ProteinsMiddle EastMolecular Sequence DataPakistanPedigreePolymorphism, Single-Stranded ConformationalSLC4A ProteinsConceptsDistal renal tubular acidosesSensorineural hearing lossNormal hearingProgressive bilateral sensorineural hearing lossBilateral sensorineural hearing lossAutosomal recessive distal renal tubular acidosisDistal renal tubular acidosisRecessive distal renal tubular acidosisSevere metabolic acidosisRenal tubular acidosisRenal tubular acidosesMetabolic acidosisTubular acidosisRenal calcificationHearing lossAlkaline urineATP6B1Distal nephronImpaired hearingApical proton pumpChildhood featuresAcidosisOne-thirdMolecular examinationHearing