Fc fusion to Glucagon-like peptide-1 inhibits degradation by human DPP-IV, increasing its half-life in serum and inducing a potent activity for human GLP-1 receptor activation

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dc.contributor.authorKim D.-M.ko
dc.contributor.authorChu S.-H.ko
dc.contributor.authorKim S.ko
dc.contributor.authorPark Y.-W.ko
dc.contributor.authorKim S.-S.ko
dc.date.accessioned2013-03-08T23:30:11Z-
dc.date.available2013-03-08T23:30:11Z-
dc.date.created2012-02-06-
dc.date.created2012-02-06-
dc.date.issued2009-
dc.identifier.citationBMB REPORTS, v.42, no.4, pp.212 - 216-
dc.identifier.issn1976-6696-
dc.identifier.urihttp://hdl.handle.net/10203/94654-
dc.description.abstractThe short in vivo half-life of GLP-1 prevents it from being used clinically. This short half-life occurs because GLP-1 is rapidly degraded by dipeptidyl peptidases such as DPP-IV. To overcome this obstacle, a GLP-1/Fc was constructed and evaluated to determine if it was degraded by DPP-IV and in serum. When the degradation of GLP-1/Fc by human DPP-IV and rabbit serum was compared with that of GLP-1 it was found to be reduced by approximately 5- and 4-fold, respectively. Furthermore, GLP-1/Fc showed a potent activity for human GLP-1 receptor activation (EC(50) approximately 6 nM). Taken together, these results indicate that GLP-1/Fc may have an extended half-life in vivo that occurs as a result of inhibition of degradation by human DPP-IV. Due to the extended half life, GLP-1/Fc may be useful for clinical treatments. [BMB reports 2009; 42(4): 212-216]-
dc.languageEnglish-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.subjectPROTEIN-KINASE-B-
dc.subjectBETA-CELLS-
dc.subjectINDUCED APOPTOSIS-
dc.subjectGROWTH-FACTOR-
dc.subjectDB/DB MICE-
dc.subjectEXPRESSION-
dc.subjectPROLIFERATION-
dc.subjectINS-1-
dc.titleFc fusion to Glucagon-like peptide-1 inhibits degradation by human DPP-IV, increasing its half-life in serum and inducing a potent activity for human GLP-1 receptor activation-
dc.typeArticle-
dc.identifier.wosid000265688500006-
dc.identifier.scopusid2-s2.0-66849101486-
dc.type.rimsART-
dc.citation.volume42-
dc.citation.issue4-
dc.citation.beginningpage212-
dc.citation.endingpage216-
dc.citation.publicationnameBMB REPORTS-
dc.contributor.nonIdAuthorChu S.-H.-
dc.contributor.nonIdAuthorKim S.-
dc.contributor.nonIdAuthorPark Y.-W.-
dc.contributor.nonIdAuthorKim S.-S.-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorDiabetes-
dc.subject.keywordAuthorDipeptidyl peptidase-IV-
dc.subject.keywordAuthorGLP-1 receptor-
dc.subject.keywordAuthorGlucagon-like peptide-1-
dc.subject.keywordAuthorIgG-Fc-
dc.subject.keywordPlusPROTEIN-KINASE-B-
dc.subject.keywordPlusBETA-CELLS-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusGROWTH-FACTOR-
dc.subject.keywordPlusDB/DB MICE-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusINS-1-
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