ReductionofCyclooxygenaseGeneDosageCounterstheOvarianMorphologicalAgingandTumorPhenotypeinWvMice
...gtheperimenopausalandimmediatepostmenopausalperiods.Thegermcell-deficientWvmicerecapitulatethesepostmenopausalalterationsinovarianmorphologyanddeveloptubularadenomas.Wedemonstratethatareductionofcyclooxygenase2genedosagerescuedtheovarianagingphenotypeoftheWvmice,whereashomozygousdeletionwasaccompani...
医源资料库;在线期刊;美国病理学杂志;2007年第169卷第4期GestationalVitaminBDeficiencyLeadstoHomocysteine-AssociatedBrainApoptosisandAltersNeurobehavioralDevelopmentinRats
【摘要】Hyperhomocysteinemiahasbeenidentifiedasariskfactorforneurologicaldisorders.Tostudytheinfluenceofearlydeficiencyinnutritionaldeterminantsofhyperhomocysteinemiaonthedevelopingratbrain,damswerefedastandarddietoradietlackingmethylgroupsduringgestationandlactation.Homocysteinemiaprogressively...
医源资料库;在线期刊;美国病理学杂志;2007年第169卷第2期AdipocytessupportcAMP-dependenttranslocationofaquaporin-2fromintracellularsitesdistinctfromtheinsulin-responsiveGLUT4storagecompartment
...3-L1adipocytes,displayscAMP-dependentplasmamembranetranslocationinamannersimilartoitsbehaviorinrenalepithelialcells.ThetranslocationofAQP2requiredphosphorylationatserine256,astheexpressionofAQP2/S256Dwasconstitutivelyplasmamembranelocalized,whereasAQP2/S256Awasrefractorytoforskolinstimulation.Unlike...
医源资料库;在线期刊;美国生理学杂志;2006年第289卷第5期Selectivesphingosine1-phosphate1receptoractivationreducesischemia-reperfusioninjuryinmousekidney
【摘要】Themechanismsinvolvedinrenalischemia-reperfusioninjury(IRI)arecomplexandappeartoinvolvetheearlyparticipationofbonemarrow-derivedcells.TlymphocytesparticipateinthepathogenesisofIRI.Sphingosine1-phosphate(S1P)inducesperipheralTcelldepletion.Therefore,wehypothesizedthatS1P1receptoractivatio...
医源资料库;在线期刊;美国生理学杂志;2006年第289卷第6期GinsenosideRg3InhibitsHumanKv1.4ChannelCurrentsbyInteractingwiththeLys531Residue
...ttoidentifythissite(s).Tothisend,wefirstassessedhowpointmutationsofvariousaminoacidresiduesofthehKv1.4channelaffectedinhibitionby20(S)-ginsenosideRg3(Rg3).Lys531residueisknowntobeakeysiteforK+activationandtobepartoftheextracellulartetraethylammonium(TEA)bindingsite;themutationK531YabolishedtheRg3eff...
医源资料库;在线期刊;分子药理学杂志;2008年第70卷第3期TransformingGrowthFactor-1ImpairsEndothelin-1-MediatedContractionofBrainVesselsbyInducingMitogen-ActivatedProtein(MAP)KinasePhosphatase-1andI
【关键词】TransformingBrainlevelsoftransforminggrowthfactor-1(TGF-1)areincreasedinAlzheimer‘sdiseaseandhavebeenimplicatedintheassociatedcerebrovascularpathology.WerecentlyreportedthattransgenicmicethatoverexpressTGF-1(TGF+mice)display,withaging,selectivelyreducedendothelin-1(ET-1)-mediatedcon...
医源资料库;在线期刊;分子药理学杂志;2007年第69卷第12期PeroxisomalProliferator-ActivatedReceptor-ProtectsRenalTubularCellsfromDoxorubicin-InducedApoptosis
...protectiveeffectofPPAR-ondoxorubicin-inducedapoptosisanditsdetailedmechanisminNRK-52Ecellsandanimalmodels.ThemRNAlevelofPPAR-wasfoundtobereducedbydoxorubicintreatmentinNRK-52Ecells.PPAR-overexpressioninNRK-52Ecellssignificantlyinhibiteddoxorubicin-inducedapoptosisandthequantityofcleavedcaspase-3.End...
医源资料库;在线期刊;分子药理学杂志;2007年第69卷第11期AntidiabetesandAntiobesityEffectofCryptotanshinoneviaActivationofAMP-ActivatedProteinKinase
...wayactivator.CryptotanshinonewasoriginallyisolatedfromthedriedrootsofSalviamilitorrhiza,anherbthatisusedextensivelyinAsianmedicineandthatisknowntoexertbeneficialeffectsonthecirculatorysystem.Forthefirsttime,inthepresentstudy,wehavedescribedthepotentantidiabeticandantiobesityeffectsofcryptotanshinone...
医源资料库;在线期刊;分子药理学杂志;2007年第69卷第7期FPProstanoidReceptor-MediatedInductionoftheExpressionofEarlyGrowthResponseFactor-1byActivationofaRas/Raf/Mitogen-ActivatedProteinKinaseSign
...tionofthehumanFPreceptorbyPGF2couldinducetheexpressionofEGR-1andfoundthat1µMPGF2producedatime-dependentinductionofbothmRNAandproteinexpressionforEGR-1.ThisFPreceptor-mediatedinductionofEGR-1expressioninvolvedactivationofthesmallGTPaseRasfollowedbyactivationofC-Rafandthemitogen-activatedprotein...
医源资料库;在线期刊;分子药理学杂志;2008年第70卷第1期InhibitionofInducibleNitric-OxideSynthaseProtectsHumanTCellsfromHypoxia-InducedApoptosis
【关键词】InhibitionSodiumcyanide-inducedchemicalhypoxiatriggersaseriesofbiochemicalalterationsleadingtoapoptosisinmanycelltypes,includingTcells.Itisknownthatchemicalhypoxiapromotesinduciblenitric-oxidesynthase(iNOS)genetranscriptionbyactivatingitstranscriptionfactors.TodeterminewhetheriNOSandN...
医源资料库;在线期刊;分子药理学杂志;2008年第70卷第3期