Expression Profiling of Human Genetic and Protein Interaction Networks in Type 1 Diabetes 英文参考文献.docVIP

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Expression Profiling of Human Genetic and Protein Interaction Networks in Type 1 Diabetes 英文参考文献.doc

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Expression Profiling of Human Genetic and Protein Interaction Networks in Type 1 Diabetes 英文参考文献

ExpressionProfilingofHumanGeneticandProtein InteractionNetworksinType1Diabetes RegineBergholdt1*,CarolineBrorsson1,KasperLage2,3,4,JensH?iriisNielsen5,S?renBrunak2, FlemmingPociot1,6,7 1Hagedorn Research Institute and Steno Diabetes Center, Gentofte, Denmark, 2Center for Biological Sequence Analysis, Technical University of Denmark, Lyngby, Denmark,3PediatricSurgicalResearchLaboratories,MassachusettsGeneralHospital,HarvardMedicalSchool,Boston,Massachusetts,UnitedStatesofAmerica,4Broad Institute of MIT and Harvard, Seven Cambridge Center, Cambridge, Massachusetts, United States of America, 5Department of Medical Biochemistry and Genetics, UniversityofCopenhagen,Copenhagen,Denmark,6UniversityofLund/ClinicalResearchCentre(CRC),Malm?,Sweden,7DepartmentofBiomedicalScience,Universityof Copenhagen,Copenhagen,Denmark Abstract Proteins contributing to a complex disease are often members of the same functional pathways. Elucidation of such pathways may provide increased knowledge about functional mechanisms underlying disease. By combining genetic interactions in Type 1 Diabetes (T1D) with protein interaction data we have previously identified sets of genes, likely to representdistinctcellularpathwaysinvolvedinT1Drisk.Hereweevaluatethecandidategenesinvolvedintheseputative interactionnetworksnotonlyatthesinglegenelevel,butalsointhecontextofthenetworksofwhichtheyformanintegral part. mRNA expression levels for each gene were evaluated and profiling was performed by measuring and comparing constitutive expression in human islets versus cytokine-stimulated expression levels, and for lymphocytes by comparing expressionlevelsamongcontrolsandT1Dindividuals.Weidentifieddifferentialregulationofseveralgenes.Inoneofthe networks four outof ninegenesshowedsignificantdown regulationin humanpancreatic isletsafter cytokine exposure supportingourpredictionthattheinteractionnetworkasawholeisariskfactor.Inaddition,wemeasuredtheenrichment ofT1DassociatedSNPsineachofthefourinteractionnetworkst