ImpairedresponsetoListeriainH2-M3–deficientmicerevealsanonredundantroleofMHCclassIb–specificTcellsinhostdefense
DepartmentofPathology,UniversityofChicago,Chicago,IL60637Themajorhistocompatibilitycomplex(MHC)classIbmoleculeH2-M3primestherapidexpansionofCD8+TcellsbypresentingN-formylatedbacterialpeptides.However,thesignificanceofH2-M3–restrictedTcellsinhostdefenseagainstbacteriaisunclear.WegeneratedH2-M3–de...
医源资料库;在线期刊;实验医学杂志;2006年第203卷第2期SrcFamilyKinaseInhibitorsBlockAmphiregulin-MediatedAutocrineErbBSignalinginNormalHumanKeratinocytes
DepartmentsofDermatology(S.K.,S.W.S.,J.L.J.,J.T.E.)andRadiationOncology(J.T.E.),UniversityofMichiganMedicalCenter,AnnArbor,MichiganAnnArborVeteransAffairsHealthSystem,AnnArbor,Michigan(J.T.E.)Abstractc-Srcpotentiatesproliferation,survival,andinvasivenessinresponsetoepidermalgrowthfactor(EGF)inhumanm...
医源资料库;在线期刊;分子药理学杂志;2005年第67卷第4期Dlgh1coordinatesactinpolymerization,synapticTcellreceptorandlipidraftaggregation,andeffectorfunctioninTcells
1DepartmentofMicrobiology,Immunology,andMolecularGenetics2MolecularBiologyInstitute,UniversityofCalifornia,LosAngeles,LosAngeles,CA900953LaJollaInstituteforAllergyandImmunology,SanDiego,CA92121Lipidraftmembranecompartmentalizationandmembrane-associatedguanylatekinase(MAGUK)familymolecularscaffoldsfu...
医源资料库;在线期刊;实验医学杂志;2005年第201卷第3期Intestinalantiinflammatoryeffectof5-aminosalicylicacidisdependentonperoxisomeproliferator–activatedreceptor-
1InstitutNationaldelaSantéetdelaRechercheMedicale(INSERM)0114,PhysiopathologiedesMaladiesInflammatoiresIntestinales,CHU59037Lille,France2INSERMU459,FacultédeMédecine,59045LilleCedex,France3InstitutdeGénétiqueetBiologieMoléculaireetCellulaire,INSERM,CentreNationaldelaRechercheScientifique,Unive...
医源资料库;在线期刊;实验医学杂志;2005年第201卷第8期ThehumanmacrophagemannosereceptordirectsMycobacteriumtuberculosislipoarabinomannan-mediatedphagosomebiogenesis
1DivisionofInfectiousDiseases,DepartmentsofInternalMedicineandMolecularVirology,Immunology,andMedicalGenetics,andtheCenterforMicrobialInterfaceBiology,TheOhioStateUniversity,Columbus,OH432102DivisionofInfectiousDiseases,DepartmentsofInternalMedicineandMicrobiology,theImmunologyProgram,andtheVAMedica...
医源资料库;在线期刊;实验医学杂志;2005年第202卷第7期LossofTumorNecrosisFactorPotentiatesTransformingGrowthFactorß-mediatedPathogenicTissueResponseduringWoundHealing
【摘要】Animalcorneaisanavasculartransparenttissuethatissuitableforresearchonwoundhealing-relatedscarringandneovascularization.Hereweshowthatlossoftumornecrosisfactor(TNF)potentiatestheundesirable,pathogenicresponseofwoundhealinginanalkali-burnedcorneainmice.Excessiveinvasionofmacrophagesandsubs...
医源资料库;在线期刊;美国病理学杂志;2006年第168卷第6期ExpressionofthehumanPAC1receptorleadstodose-dependenthydrocephalus-relatedabnormalitiesinmice
1SchoolofMedicalSciences,InstituteofMedicalSciences,UniversityofAberdeen,Aberdeen,UnitedKingdom.2UltrasoundDepartment,AberdeenMaternityHospital,GrampianUniversityHospitalsNHSTrust,Aberdeen,UnitedKingdom.3CentreforNeuroscienceResearch,SchoolofBiomedicalSciences,UniversityofEdinburgh,Edinburgh,UnitedK...
医源资料库;在线期刊;临床研究杂志;2006年第116卷第7期MetalloproteinasesMediateMucin5ACExpressionbyEpidermalGrowthFactorReceptorActivation
DepartmentsofEnvironmentalHealthandPulmonaryandCriticalCareMedicine,UniversityofCincinnati,Cincinnati,OhioDepartmentofMolecularBiomedicalSciences,CollegeofVeterinaryMedicine,NorthCarolinaStateUniversity,Raleigh,NorthCarolinaCardiovascularResearchInstituteandDepartmentsofMedicineandPhysiology,Univers...
医源资料库;在线期刊;美国呼吸和危急护理医学;2005年第171卷第2期PioglitazoneInhibitsAndrogenProductioninNCI-H295RCellsbyRegulatingGeneExpressionofCYP17andHSD3B2
...nediones(TZDs)suchaspioglitazoneandrosiglitazonearewidelyusedasinsulinsensitizersinthetreatmentoftype2diabetes.Indiabeticwomenwithpolycysticovarysyndrome,treatmentwithpioglitazoneorrosiglitazoneimprovesinsulinresistanceandhyperandrogenism,butthemechanismbywhichTZDsdown-regulateandrogenproductionisun...
医源资料库;在线期刊;分子药理学杂志;2007年第69卷第3期Anti-IL-23therapyinhibitsmultipleinflammatorypathwaysandamelioratesautoimmuneencephalomyelitis
...ProteinEngineering,Schering-PloughBiopharma,PaloAlto,California,USA.AbstractIL-23isamemberoftheIL-12cytokinefamilythatdrivesahighlypathogenicTcellpopulationinvolvedintheinitiationofautoimmunediseases.WehaveshownthatIL-23–dependent,pathogenicTcellsproducedIL-17A,IL-17F,IL-6,andTNFbutnotIFN-orIL-4.W...
医源资料库;在线期刊;临床研究杂志;2006年第116卷第5期