2011
Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria
Guo JK, Marlier A, Shi H, Shan A, Ardito TA, Du ZP, Kashgarian M, Krause DS, Biemesderfer D, Cantley LG. Increased Tubular Proliferation as an Adaptive Response to Glomerular Albuminuria. Journal Of The American Society Of Nephrology 2011, 23: 429-437. PMID: 22193389, PMCID: PMC3294312, DOI: 10.1681/asn.2011040396.Peer-Reviewed Original ResearchMeSH KeywordsAlbuminuriaAnimalsAxl Receptor Tyrosine KinaseCell ProliferationDisease Models, AnimalFemaleHeparin-binding EGF-like Growth FactorIntegrasesIntercellular Signaling Peptides and ProteinsIntracellular Signaling Peptides and ProteinsKidney GlomerulusKidney Tubules, ProximalMaleMembrane ProteinsMiceMice, TransgenicPodocytesProteinuriaProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesConceptsGlomerular proteinuriaTubular injuryTubular proliferationStructural glomerular injuryProteinuric renal diseaseOnset of albuminuriaRenal tubular atrophyDiphtheria toxin receptorRenal tubular cellsProximal tubule cellsGlomerular albuminuriaRenal failureSystemic inflammationTubular damageProgressive glomerulosclerosisRenal diseaseTubular atrophyGlomerular injuryRenal responsePodocyte lossProliferative responseTubular cellsAnimal modelsProteinuriaReceptor Axl
2006
An Inducible Mouse Model for PAX2-Dependent Glomerular Disease: Insights into a Complex Pathogenesis
Wagner KD, Wagner N, Guo JK, Elger M, Dallman MJ, Bugeon L, Schedl A. An Inducible Mouse Model for PAX2-Dependent Glomerular Disease: Insights into a Complex Pathogenesis. Current Biology 2006, 16: 793-800. PMID: 16631587, DOI: 10.1016/j.cub.2006.02.072.Peer-Reviewed Original ResearchConceptsInducible mouse modelGlomerular diseaseMouse modelAngiotensin-converting enzyme inhibitorEnd-stage renal failureTreatment of miceHealthy adult animalsRenal failureRenal functionRenal diseaseComplex pathogenesisNephrin expressionEnzyme inhibitorsDiseaseAdult animalsPodocytesDedifferentiated phenotypePersistent expressionMature podocytesPAX2MicePax genesFunctional relevanceTranscriptional repressorActivation
2002
Early Gonadal Development: Exploring Wt1 and Sox9 Function
Guo J, Hammes A, Chaboissier M, Vidal V, Xing Y, Wong F, Schedl A. Early Gonadal Development: Exploring Wt1 and Sox9 Function. Novartis Foundation Symposia 2002, 244: 23-34. PMID: 11990794, DOI: 10.1002/0470868732.ch3.Peer-Reviewed Original ResearchConceptsSox9 functionSex determinationSex-determining gene SRYSex-determining signalWilms' tumor suppressorFemale sex reversalBipotential primordiumGonad formationGene SRYXX gonadsTransgenic experimentsFirst geneGonadal primordiumMouse developmentPosttranscriptional modificationsKnockout experimentsSex reversalHuman SOX9Distinct functionsSRY geneGonadal anlageSOX9 geneTumor suppressorImportant regulatorGenes
2001
Two Splice Variants of the Wilms' Tumor 1 Gene Have Distinct Functions during Sex Determination and Nephron Formation
Hammes A, Guo J, Lutsch G, Leheste J, Landrock D, Ziegler U, Gubler M, Schedl A. Two Splice Variants of the Wilms' Tumor 1 Gene Have Distinct Functions during Sex Determination and Nephron Formation. Cell 2001, 106: 319-329. PMID: 11509181, DOI: 10.1016/s0092-8674(01)00453-6.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAlternative SplicingAnimalsAnimals, NewbornApoptosisBase SequenceCell SurvivalDAX-1 Orphan Nuclear ReceptorDisorders of Sex DevelopmentDNA-Binding ProteinsExonsFemaleGenes, Wilms TumorGlomerulosclerosis, Focal SegmentalGonadsMaleMiceMutagenesisNephronsNuclear ProteinsProtein IsoformsReceptors, Retinoic AcidRepressor ProteinsRNA Splice SitesRNA, MessengerSex Determination ProcessesSex-Determining Region Y ProteinSyndromeTranscription FactorsWT1 ProteinsConceptsTumor 1 geneDistinct functionsKTS isoformsSex determination pathwaySplice variantsDistinct molecular functionsZinc finger 3XY sex reversalWilms' tumor 1 geneMolecular functionsWT1 resultsAlternative splicingSex determinationSex reversalFinger 3Nephron formationHomozygous mutantsSpecific isoformsImportant regulatorExpression levelsIsoformsKidney defectsFrasier syndromeHeterozygous miceMouse strains