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Cited 17 times in

Lysosomal trafficking of TGFBIp via caveolae-mediated endocytosis

DC FieldValueLanguage
dc.contributor.author김응권-
dc.contributor.author김태임-
dc.contributor.author맹용선-
dc.contributor.author최승일-
dc.date.accessioned2016-02-04T11:14:20Z-
dc.date.available2016-02-04T11:14:20Z-
dc.date.issued2015-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139975-
dc.description.abstractTransforming growth factor-beta-induced protein (TGFBIp) is ubiquitously expressed in the extracellular matrix (ECM) of various tissues and cell lines. Progressive accumulation of mutant TGFBIp is directly involved in the pathogenesis of TGFBI-linked corneal dystrophy. Recent studies reported that mutant TGFBIp accumulates in cells; however, the trafficking of TGFBIp is poorly understood. Therefore, we investigated TGFBIp trafficking to determine the route of its internalization and secretion and to elucidate its roles in the pathogenesis of granular corneal dystrophy type 2 (GCD2). Our data indicate that newly synthesized TGFBIp was secreted via the endoplasmic reticulum/Golgi-dependent secretory pathway, and this secretion was delayed in the corneal fibroblasts of patients with GCD2. We also found that TGFBIp was internalized by caveolae-mediated endocytosis, and the internalized TGFBIp accumulated after treatment with bafilomycin A1, an inhibitor of lysosomal degradation. In addition, the proteasome inhibitor MG132 inhibits the endocytosis of TGFBIp. Co-immunoprecipitation revealed that TGFBIp interacted with integrin αVβ3. Moreover, treatment with arginine-glycine-aspartic acid (RGD) tripeptide suppressed the internalization of TGFBIp. These insights on TGFBIp trafficking could lead to the identification of novel targets and the development of new therapies for TGFBI-linked corneal dystrophy.-
dc.description.statementOfResponsibilityopen-
dc.format.extente0119561-
dc.relation.isPartOfPLOS ONE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdolescent-
dc.subject.MESHAdult-
dc.subject.MESHAmino Acid Motifs-
dc.subject.MESHCaveolae/metabolism*-
dc.subject.MESHChild-
dc.subject.MESHCorneal Diseases/pathology-
dc.subject.MESHEndocytosis*-
dc.subject.MESHEndoplasmic Reticulum/metabolism-
dc.subject.MESHExtracellular Matrix Proteins/chemistry-
dc.subject.MESHExtracellular Matrix Proteins/metabolism*-
dc.subject.MESHFemale-
dc.subject.MESHFibroblasts/cytology-
dc.subject.MESHFibroblasts/pathology-
dc.subject.MESHGolgi Apparatus/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHIntegrin alphaVbeta3/metabolism-
dc.subject.MESHLysosomes/metabolism*-
dc.subject.MESHMale-
dc.subject.MESHProteasome Endopeptidase Complex/metabolism-
dc.subject.MESHProteolysis-
dc.subject.MESHTransforming Growth Factor beta/chemistry-
dc.subject.MESHTransforming Growth Factor beta/metabolism*-
dc.subject.MESHUbiquitin/metabolism-
dc.subject.MESHYoung Adult-
dc.titleLysosomal trafficking of TGFBIp via caveolae-mediated endocytosis-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Ophthalmology (안과학)-
dc.contributor.googleauthorSeung-il Choi-
dc.contributor.googleauthorYong-Sun Maeng-
dc.contributor.googleauthorTae-im Kim-
dc.contributor.googleauthorYangsin Lee-
dc.contributor.googleauthorYong-Sun Kim-
dc.contributor.googleauthorEung Kweon Kim-
dc.identifier.doi10.1371/journal.pone.0119561-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00831-
dc.contributor.localIdA01080-
dc.contributor.localIdA01346-
dc.contributor.localIdA04099-
dc.relation.journalcodeJ02540-
dc.identifier.eissn1932-6203-
dc.identifier.pmid25853243-
dc.contributor.alternativeNameKim, Eung Kweon-
dc.contributor.alternativeNameKim, Tae Im-
dc.contributor.alternativeNameMaeng, Yong Sun-
dc.contributor.alternativeNameChoi, Seung Il-
dc.contributor.affiliatedAuthorKim, Eung Kweon-
dc.contributor.affiliatedAuthorKim, Tae Im-
dc.contributor.affiliatedAuthorMaeng, Yong Sun-
dc.contributor.affiliatedAuthorChoi, Seung Il-
dc.rights.accessRightsfree-
dc.citation.volume10-
dc.citation.number4-
dc.citation.startPagee0119561-
dc.identifier.bibliographicCitationPLOS ONE, Vol.10(4) : e0119561, 2015-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Corneal Dystrophy Research Institute (각막이상증연구소) > 1. Journal Papers

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