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Synaptic scaffolding molecule binds to and regulates vasoactive intestinal polypeptide type-1 receptor in epithelial cells.

DC Field Value Language
dc.contributor.author김경식-
dc.contributor.author김경환-
dc.contributor.author김주영-
dc.contributor.author김호근-
dc.contributor.author박현우-
dc.contributor.author이민구-
dc.date.accessioned2015-04-24T16:48:36Z-
dc.date.available2015-04-24T16:48:36Z-
dc.date.issued2009-
dc.identifier.issn0016-5085-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/104213-
dc.description.abstractBACKGROUND & AIMS: Vasoactive intestinal polypeptide (VIP) is a principal regulator of fluid and electrolyte secretion in the gastrointestinal system. The VIP type-1 receptor (VPAC1), a class II G-protein-coupled receptor, contains a putative C-terminal PDZ-binding motif. A yeast 2-hybrid screen indicated that the C-terminus of VPAC1 bound to the PDZ domain of synaptic scaffolding molecule (S-SCAM, also known as membrane-associated guanylate kinase inverted-2 [MAGI-2]). We analyzed the association between S-SCAM and VPAC1. METHODS: The biochemical properties and physiologic significance of the interaction between VPAC1 and S-SCAM were examined in heterologous expression systems, T84 colonic epithelial cells, and human pancreas and colon tissues using an integrated molecular and physiologic approach. RESULTS: The physical interaction between VPAC1 and S-SCAM was confirmed by immunoprecipitation in HEK 293 mammalian cells and human pancreatic and colonic tissues. Immunocytochemical analysis indicated that S-SCAM recruited VPAC1 to the junctional area near the apical end of the lateral membrane in T84 cells. Several lines of evidence revealed that S-SCAM inhibits VPAC1 activation. Overexpression of S-SCAM inhibited VPAC1-mediated cAMP production and agonist-induced VPAC1 internalization in HEK 293 and HeLa cells. In addition, S-SCAM decreased the VPAC1-mediated current through the cystic fibrosis transmembrane conductance regulator in Xenopus oocytes, especially at low concentrations of VIP. Importantly, loss of S-SCAM increased VIP-induced short-circuit currents in T84 monolayers, which endogenously express VPAC1 and S-SCAM. CONCLUSIONS: S-SCAM/MAGI-2 interacts with and regulates VPAC1 intracellular localization in epithelial cells and inhibits VPAC1 agonist-induced activation and internalization.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfGASTROENTEROLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnalysis of Variance-
dc.subject.MESHCarrier Proteins-
dc.subject.MESHCell Communication/genetics-
dc.subject.MESHCell Communication/physiology-
dc.subject.MESHCells, Cultured-
dc.subject.MESHEpithelial Cells/metabolism*-
dc.subject.MESHEpithelial Cells/physiology-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHHumans-
dc.subject.MESHImmunoblotting-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHProbability-
dc.subject.MESHProtein Binding/genetics-
dc.subject.MESHProtein Binding/physiology*-
dc.subject.MESHReceptors, Vasoactive Intestinal Polypeptide, Type I/genetics-
dc.subject.MESHReceptors, Vasoactive Intestinal Polypeptide, Type I/metabolism*-
dc.subject.MESHSignal Transduction/genetics-
dc.subject.MESHTwo-Hybrid System Techniques-
dc.titleSynaptic scaffolding molecule binds to and regulates vasoactive intestinal polypeptide type-1 receptor in epithelial cells.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Surgery (외과학)-
dc.contributor.googleauthorHEON YUNG GEE-
dc.contributor.googleauthorYOUNG WOONG KIM-
dc.contributor.googleauthorMIN JAE JO-
dc.contributor.googleauthorWAN NAMKUNG-
dc.contributor.googleauthorJOO YOUNG KIM-
dc.contributor.googleauthorHYUN WOO PARK-
dc.contributor.googleauthorKYUNG SIK KIM-
dc.contributor.googleauthorHOGUEN KIM-
dc.contributor.googleauthorAKEMICHI BABA-
dc.contributor.googleauthorJINHEE YANG-
dc.contributor.googleauthorEUNJOON KIM-
dc.contributor.googleauthorKYUNG HWAN KIM-
dc.contributor.googleauthorMIN GOO LEE-
dc.identifier.doi10.1053/j.gastro.2009.01.065-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00942-
dc.contributor.localIdA00299-
dc.contributor.localIdA00311-
dc.contributor.localIdA01183-
dc.contributor.localIdA01743-
dc.contributor.localIdA02781-
dc.contributor.localIdA03971-
dc.relation.journalcodeJ00917-
dc.identifier.eissn1528-0012-
dc.identifier.pmid19642226-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0016508509001693-
dc.contributor.alternativeNameKim, Kyung Sik-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.alternativeNameKim, Joo Young-
dc.contributor.alternativeNameKim, Ho Keun-
dc.contributor.alternativeNamePark, Hyun Woo-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.affiliatedAuthorKim, Joo Young-
dc.contributor.affiliatedAuthorKim, Kyung Sik-
dc.contributor.affiliatedAuthorKim, Kyung Hwan-
dc.contributor.affiliatedAuthorKim, Ho Keun-
dc.contributor.affiliatedAuthorPark, Hyun Woo-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorGee, Heon Yung-
dc.citation.volume137-
dc.citation.number2-
dc.citation.startPage607-
dc.citation.endPage617.e4-
dc.identifier.bibliographicCitationGASTROENTEROLOGY, Vol.137(2) : 607-617.e4, 2009-
dc.identifier.rimsid56116-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers

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