2000
G1 kinases and transforming growth factor-β; signaling are associated with a growth pattern switch in diabetes-induced renal growth
Huang H, Preisig P. G1 kinases and transforming growth factor-β; signaling are associated with a growth pattern switch in diabetes-induced renal growth. Kidney International 2000, 58: 162-172. PMID: 10886561, DOI: 10.1046/j.1523-1755.2000.00151.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCDC2-CDC28 KinasesCyclin ECyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent KinasesDiabetes Mellitus, ExperimentalDiabetic NephropathiesDNA-Binding ProteinsG1 PhaseHyperplasiaHypertrophyKidney Tubules, ProximalMaleProtein Serine-Threonine KinasesProto-Oncogene ProteinsRatsRats, Sprague-DawleyReceptors, Transforming Growth Factor betaSignal TransductionSmad2 ProteinSmad4 ProteinTrans-ActivatorsTransforming Growth Factor betaConceptsReceptor II expressionCyclin E kinase activityReceptor expressionRenal growthGrowth factor beta receptor expressionTGF-beta receptor II expressionBaseline levelsProximal tubule cell growthTGF-beta receptor expressionBody weight ratioCdk2/cyclin E kinase activityCdk2/cyclin E complexesCyclin DRenal proximal tubulesDiabetes mellitusDiabetic ratsTGF-beta signalingDiabetic stateCyclin E complexGrowth patternDay 2Proximal tubulesDay 4Day 10Tubule growth
1999
Size does matter: Will knockout of p21WAF1/CIP1 save the kidney by limiting compensatory renal growth?
Al-Awqati Q, Preisig P. Size does matter: Will knockout of p21WAF1/CIP1 save the kidney by limiting compensatory renal growth? Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 10551-10553. PMID: 10485857, PMCID: PMC33735, DOI: 10.1073/pnas.96.19.10551.Peer-Reviewed Original ResearchTGF-β1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase
Liu B, Preisig P. TGF-β1-mediated hypertrophy involves inhibiting pRB phosphorylation by blocking activation of cyclin E kinase. American Journal Of Physiology 1999, 277: f186-f194. PMID: 10444572, DOI: 10.1152/ajprenal.1999.277.2.f186.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCdc25 PhosphatasesCDC2-CDC28 KinasesCell Cycle ProteinsCell LineCyclin ECyclin-Dependent Kinase 2Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent Kinase Inhibitor p57Cyclin-Dependent KinasesEnzyme ActivationEpidermal Growth FactorHypertrophyKidneyMicrotubule-Associated ProteinsNuclear ProteinsPhosphorylationProtein Serine-Threonine KinasesProtein Tyrosine PhosphatasesProto-Oncogene ProteinsRatsRetinoblastoma ProteinTransforming Growth Factor betaTumor Suppressor ProteinsConceptsCdk2/cyclin E complexesCyclin E complexCyclin E kinaseGrowth responseE complexCell cycle progressionRenal epithelial cellsProtein abundanceRetinoblastoma proteinKinase activityCycle progressionHypophosphorylated statePRB phosphorylationHypertrophic growth responseKinaseCyclin EAbundanceEpithelial cellsActive stateDevelopment of hypertrophyActivationCell entranceComplexesArrestTGF-β1