Dysbindin Regulates the Transcriptional Level of Myristoylated Alanine-Rich Protein Kinase C Substrate via the Interaction with NF-YB in Mice Brain 英文参考文献.docVIP

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Dysbindin Regulates the Transcriptional Level of Myristoylated Alanine-Rich Protein Kinase C Substrate via the Interaction with NF-YB in Mice Brain 英文参考文献.doc

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Dysbindin Regulates the Transcriptional Level of Myristoylated Alanine-Rich Protein Kinase C Substrate via the Interaction with NF-YB in Mice Brain 英文参考文献

DysbindinRegulatestheTranscriptionalLevelof MyristoylatedAlanine-RichProteinKinaseCSubstrate viatheInteractionwithNF-YBinMiceBrain HiroakiOkuda1,2.,RyusukeKuwahara1.,ShinsukeMatsuzaki1,3,4.*,ShingoMiyata1,3 ,Natsuko Kumamoto1,TsuyoshiHattori1,3,ShokoShimizu1,KoheiYamada1,KeisukeKawamoto1 ,Ryota Hashimoto3,5,MasatoshiTakeda5,TaiichiKatayama4,MasayaTohyama1,3,4 1DepartmentofAnatomyandNeuroscience,GraduateSchoolofMedicine,OsakaUniversity,Osaka,Japan,2DepartmentofSecondAnatomy,FacultyofMedicine,Nara MedicalUniversity,Nara,Japan,3TheOsaka-HamamatsuJointResearchCenterforChildMentalDevelopment,GraduateSchoolofMedicine,OsakaUniversity,Osaka, Japan, 4Department of Child Development and Molecular Brain Science, United Graduate School of Child Development, Osaka University, Kanazawa University and HamamatsuUniversitySchoolofMedicine,Osaka,Japan,5DepartmentofPsychiatry,OsakaUniversityGraduateSchoolofMedicine,Osaka,Japan Abstract Background: An accumulating body of evidence suggests that Dtnbp1 (Dysbindin) is a key susceptibility gene for schizophrenia. Using the yeast-two-hybrid screening system, we examined the candidate proteins interacting with DysbindinandrevealedoneofthesecandidatestobethetranscriptionfactorNF-YB. Methods: We employed an immunoprecipitation (IP) assay to demonstrate the Dysbindin-NF-YB interaction. DNA chips were used to screen for altered expression of genes in cells in which Dysbindin or NF-YB was down regulated, while ChromatinIPandReporterassayswereusedtoconfirmtheinvolvementofthesegenesintranscriptionofMyristoylated alanine-rich protein kinase C substrate (MARCKS). The sdy mutant mice with a deletion in Dysbindin, which exhibit behavioralabnormalities,andwild-typeDBA2JmicewereusedtoinvestigateMARCKSexpression. Results: We revealed an interaction between Dysbindin and NF-YB. DNA chips showed that MARCKS expression was increasedinbothDysbindinknockdowncellsandNF-YBknockdowncells,andChromatinIPrevealedinteractionofthese proteins at the MARCKS promoter re