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http://purl.uniprot.org/citations/17560942http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17560942http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17560942http://www.w3.org/2000/01/rdf-schema#comment"The unfolded protein response (UPR) is a conserved and adaptive cellular response to increase cell survival during ER stress. XBP-1 spliced form (XBP-1S) generated by IRE1 endoribonuclease is a key transcriptional regulator in UPR to activate genes involved in protein folding and degradation to restore ER function. Although Akt activation was suggested to be a pro-survival pathway activated during ER stress, the signal to trigger Akt is still not clear. In this study, we report IGF1 transcription and Akt phosphorylation are enhanced in XBP-1S stably overexpressed clone of zebrafish embryonic cell line (ZF4). In addition, zebrafish IGF1 intron1 with predicted UPRE (XBP-1S binding sites) and ERSE (ATF6/XBP-1S binding site) linked with basal promoter could be activated by XBP-1S, not by XBP-1 unspliced form (XBP-1U). Furthermore, we demonstrate that expression of endogenous IGF1 is transiently induced as XBP-1 splicing during ER stress in parallel to ER chaperone GRP78/Hspa5 and ER resided E3 ubiquitin ligase Synoviolin in ZF4 cells by quantitative PCR. Our results suggest zebrafish XBP-1S not only activates genes responsible for protein folding, transporting, glycosylation and ER associated degradation but also activates anti-apoptosis signal via IGF1/Akt pathway in unfolded protein response to cope with ER stress."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.org/dc/terms/identifier"doi:10.1016/j.bbrc.2007.05.183"xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Wu J.L."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Wu J.L."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Chen M.H."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Chen M.H."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Gong H.Y."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Gong H.Y."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Hu M.C."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Hu M.C."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Lin G.H."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Lin G.H."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Huang S.J."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Huang S.J."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Liao C.F."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Liao C.F."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Hu S.Y."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/author"Hu S.Y."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/name"Biochem. Biophys. Res. Commun."xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/name"Biochem Biophys Res Commun"xsd:string
http://purl.uniprot.org/citations/17560942http://purl.uniprot.org/core/pages"778-783"xsd:string