2018
Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment
Lee Y, Blount KL, Dai F, Thompson S, Scher JK, Bitterman S, Droher M, Herzog EL, Moeckel G, Karihaloo A, Dahl NK. Semaphorin 7A in circulating regulatory T cells is increased in autosomal-dominant polycystic kidney disease and decreases with tolvaptan treatment. Clinical And Experimental Nephrology 2018, 22: 906-916. PMID: 29453607, DOI: 10.1007/s10157-018-1542-x.Peer-Reviewed Original ResearchConceptsPeripheral blood mononuclear cellsAutosomal dominant polycystic kidney diseaseEnd-stage renal diseaseRenal fibrosisSEMA7A expressionADPKD patientsTolvaptan treatmentPolycystic kidney diseaseKidney diseaseNumber of PBMCsExpression of SEMA7ASubsequent renal fibrosisMarkers of inflammationRegulatory T cellsADPKD kidneysBlood mononuclear cellsImmunomodulating proteinsRenal diseaseMononuclear cellsSmall kidneysKidney fibrosisLiver fibrosisRenal cystsSemaphorin 7AT cells
2012
Evaluation of urine biomarkers of kidney injury in polycystic kidney disease
Parikh CR, Dahl NK, Chapman AB, Bost JE, Edelstein CL, Comer DM, Zeltner R, Tian X, Grantham JJ, Somlo S. Evaluation of urine biomarkers of kidney injury in polycystic kidney disease. Kidney International 2012, 81: 784-790. PMID: 22258321, PMCID: PMC3319327, DOI: 10.1038/ki.2011.465.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAdultAnimalsBiomarkersDisease ProgressionFemaleHumansInterleukin-18KidneyKidney Failure, ChronicLipocalin-2LipocalinsLongitudinal StudiesMaleMiceMice, KnockoutMice, TransgenicOncogene ProteinsPolycystic Kidney, Autosomal DominantProto-Oncogene ProteinsRatsRats, Mutant StrainsRats, Sprague-DawleyReceptors, Interleukin-18TRPP Cation ChannelsConceptsAutosomal dominant polycystic kidney diseaseTotal kidney volumeKidney volumeIL-18Polycystic kidney diseaseKidney diseaseCyst fluidRenal tubular integrityIL-18 levelsRenal Disease equationSerial urine samplesGlomerular filtration rateModification of DietExpression of Lcn2Min/yearPolycystic Kidney Disease (CRISP) studyUrine of patientsDominant polycystic kidney diseaseKidney Disease studyUrinary collecting systemMean percentage increaseSPRD rat modelUrinary NGALUrine NGALKidney injury
2003
Deficient HCO 3 - Transport in an AE1 Mutant with Normal Cl- Transport Can be Rescued by Carbonic Anhydrase II Presented on an Adjacent AE1 Protomer*
Dahl NK, Jiang L, Chernova MN, Stuart-Tilley AK, Shmukler BE, Alper SL. Deficient HCO 3 - Transport in an AE1 Mutant with Normal Cl- Transport Can be Rescued by Carbonic Anhydrase II Presented on an Adjacent AE1 Protomer*. Journal Of Biological Chemistry 2003, 278: 44949-44958. PMID: 12933803, DOI: 10.1074/jbc.m308660200.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAnion Exchange Protein 1, ErythrocyteAnionsBicarbonatesBinding SitesBiological TransportCarbonic Anhydrase IIChloridesDimerizationFemaleGene DeletionGene ExpressionHumansLipid BilayersMiceMolecular Sequence DataMutagenesisMutation, MissenseOocytesProtein SubunitsStructure-Activity RelationshipTransfectionXenopusConceptsCl-/HCO3- exchange activityPrevention of Ca2Normal CLCl-/HCO3II inhibitionHCO3- transportIntracellular HCO3Missense mutationsCytoplasmic tailC-terminal cytoplasmic tailXenopus oocytesCa2Binding sitesCl transportAE1InhibitionIntact Ca2Minimal extentCarbonic anhydrase IIActivityMissense mutantsPathwayAE1 mutantsExchange activity