DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kim D.-M. | ko |
dc.contributor.author | Chu S.-H. | ko |
dc.contributor.author | Kim S. | ko |
dc.contributor.author | Park Y.-W. | ko |
dc.contributor.author | Kim S.-S. | ko |
dc.date.accessioned | 2013-03-08T23:30:11Z | - |
dc.date.available | 2013-03-08T23:30:11Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | BMB REPORTS, v.42, no.4, pp.212 - 216 | - |
dc.identifier.issn | 1976-6696 | - |
dc.identifier.uri | http://hdl.handle.net/10203/94654 | - |
dc.description.abstract | The 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.language | English | - |
dc.publisher | KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY | - |
dc.subject | PROTEIN-KINASE-B | - |
dc.subject | BETA-CELLS | - |
dc.subject | INDUCED APOPTOSIS | - |
dc.subject | GROWTH-FACTOR | - |
dc.subject | DB/DB MICE | - |
dc.subject | EXPRESSION | - |
dc.subject | PROLIFERATION | - |
dc.subject | INS-1 | - |
dc.title | 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 | - |
dc.type | Article | - |
dc.identifier.wosid | 000265688500006 | - |
dc.identifier.scopusid | 2-s2.0-66849101486 | - |
dc.type.rims | ART | - |
dc.citation.volume | 42 | - |
dc.citation.issue | 4 | - |
dc.citation.beginningpage | 212 | - |
dc.citation.endingpage | 216 | - |
dc.citation.publicationname | BMB REPORTS | - |
dc.contributor.nonIdAuthor | Chu S.-H. | - |
dc.contributor.nonIdAuthor | Kim S. | - |
dc.contributor.nonIdAuthor | Park Y.-W. | - |
dc.contributor.nonIdAuthor | Kim S.-S. | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | Diabetes | - |
dc.subject.keywordAuthor | Dipeptidyl peptidase-IV | - |
dc.subject.keywordAuthor | GLP-1 receptor | - |
dc.subject.keywordAuthor | Glucagon-like peptide-1 | - |
dc.subject.keywordAuthor | IgG-Fc | - |
dc.subject.keywordPlus | PROTEIN-KINASE-B | - |
dc.subject.keywordPlus | BETA-CELLS | - |
dc.subject.keywordPlus | INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | GROWTH-FACTOR | - |
dc.subject.keywordPlus | DB/DB MICE | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | INS-1 | - |
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