dc.creatorFURUYA, Daniela Tomie
dc.creatorISHII, Tatsuya
dc.creatorKAMIKAWA, Akihiro
dc.creatorSHIMADA, Kohei
dc.creatorMACHADO, Ubiratan Fabres
dc.creatorSAITO, Masayuki
dc.creatorKIMURA, Kazuhiro
dc.date.accessioned2012-10-20T03:18:41Z
dc.date.accessioned2018-07-04T15:34:47Z
dc.date.available2012-10-20T03:18:41Z
dc.date.available2018-07-04T15:34:47Z
dc.date.created2012-10-20T03:18:41Z
dc.date.issued2009
dc.identifierJAPANESE JOURNAL OF VETERINARY RESEARCH, v.57, n.3, p.163-167, 2009
dc.identifier0047-1917
dc.identifierhttp://producao.usp.br/handle/BDPI/28059
dc.identifierhttp://apps.isiknowledge.com/InboundService.do?Func=Frame&product=WOS&action=retrieve&SrcApp=EndNote&UT=000272640800003&Init=Yes&SrcAuth=ResearchSoft&mode=FullRecord
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1624703
dc.description.abstractTo characterize the roles of C-peptide in vascular homeostatic processes, we examined the genes regulated by C-peptide in LEII mouse lung microvascular endothelial cells. Treatment of the cells with C-peptide increased the expression of c-Jun N-terminal kinase 1 (JNK1) mRNA dose-dependently, accompanied by an increase in JNK1 protein content. Prior treatment of the cells with PD98059, an ERK kinase inhibitor or SB203580, a p38MAPK inhibitor, abrogated the C-peptide-elicited JNK1 mRNA expression. These results indicate that C-peptide increases JNK1 protein levels, possibly through ERK- and p38MAPK-dependent activation of JNK. gene transcription.
dc.languageeng
dc.publisherHOKKAIDO UNIV
dc.relationJapanese Journal of Veterinary Research
dc.rightsCopyright HOKKAIDO UNIV
dc.rightsrestrictedAccess
dc.subjectC-peptide
dc.subjectdiabetes mellitus
dc.subjectJNK
dc.titleProinsulin C-peptide induces c-Jun N-terminal kinase 1 expression in LEII mouse lung capillary endothelial cells
dc.typeArtículos de revistas


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