Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/49178
Campo DC Valoridioma
dc.contributor.authorMartin, Danielen_US
dc.contributor.authorRojo, Ana I.en_US
dc.contributor.authorSalinas, Martaen_US
dc.contributor.authorDiaz, Raquelen_US
dc.contributor.authorGallardo, Germanen_US
dc.contributor.authorAlam, Jaweden_US
dc.contributor.authorRuiz De Galarreta Hernandez,C. Manuelen_US
dc.contributor.authorCuadrado, Antonioen_US
dc.date.accessioned2018-11-24T04:54:33Z-
dc.date.available2018-11-24T04:54:33Z-
dc.date.issued2004en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10553/49178-
dc.description.abstractThe phosphatidylinositol 3-kinase (PI3K)/Akt pathway elicits a survival signal against multiple apoptotic insults. In addition, phase II enzymes such as heme oxygenase-1 (HO-1) protect cells against diverse toxins and oxidative stress. In this work, we describe a link between these defense systems at the level of transcriptional regulation of the antioxidant enzyme HO-1. The herb-derived phenol carnosol induced HO-1 expression at both mRNA and protein levels. Luciferase reporter assays indicated that carnosol targeted the mouse ho1 promoter at two enhancer regions comprising the antioxidant response elements (AREs). Moreover, carnosol increased the nuclear levels of Nrf2, a transcription factor governing AREs. Electrophoretic mobility shift assays and luciferase reporter assays with a dominant-negative Nrf2 mutant indicated that carnosol increased the binding of Nrf2 to ARE and induced Nrf2-dependent activation of the ho1 promoter. While investigating the signaling pathways responsible for HO-1 induction, we observed that carnosol activated the ERK, p38, and JNK pathways as well as the survival pathway driven by PI3K. Inhibition of PI3K reduced the increase in Nrf2 protein levels and activation of the ho1 promoter. Expression of active PI3K-CAAX ( where A is aliphatic amino acid) was sufficient to activate AREs. The use of dominant-negative mutants of protein kinase Czeta and Akt1, two kinases downstream from PI3K, demonstrated a requirement for active Akt1, but not protein kinase Czeta. Moreover, the long-term antioxidant effect of carnosol was partially blocked by PI3K or HO-1 inhibitors, further demonstrating that carnosol attenuates oxidative stress through a pathway that involves PI3K and HO-1.en_US
dc.languageengen_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.sourceJournal of Biological Chemistry[ISSN 0021-9258],v. 279, p. 8919-8929en_US
dc.subject32 Ciencias médicasen_US
dc.subject2302 Bioquímicaen_US
dc.subject.otherProtein-Kinase-Cen_US
dc.subject.otherRenal Epithelial-Cellsen_US
dc.subject.otherOxidative Stressen_US
dc.subject.otherGene-Expressionen_US
dc.subject.otherNf-E2-Related Factor-2en_US
dc.subject.otherEndothelial-Cellsen_US
dc.subject.otherPrimary Culturesen_US
dc.subject.otherRat Hepatocytesen_US
dc.subject.otherSodium Arseniteen_US
dc.subject.otherInductionen_US
dc.titleRegulation of Heme Oxygenase-1 Expression through the Phosphatidylinositol 3-Kinase/Akt Pathway and the Nrf2 Transcription Factor in Response to the Antioxidant Phytochemical Carnosolen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1074/jbc.M309660200en_US
dc.identifier.scopus1542335553-
dc.identifier.isi000189265900050-
dc.contributor.authorscopusid56484788100-
dc.contributor.authorscopusid7005764407-
dc.contributor.authorscopusid7006754360-
dc.contributor.authorscopusid7201925856-
dc.contributor.authorscopusid57197332997-
dc.contributor.authorscopusid6603046608-
dc.contributor.authorscopusid7102958617-
dc.contributor.authorscopusid7003806034-
dc.contributor.authorscopusid7005588564-
dc.description.lastpage8929en_US
dc.description.firstpage8919en_US
dc.relation.volume279en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid1575213-
dc.contributor.daisngid330184-
dc.contributor.daisngid9538013-
dc.contributor.daisngid11977739-
dc.contributor.daisngid7801524-
dc.contributor.daisngid102954-
dc.contributor.daisngid1664323-
dc.contributor.daisngid29362754-
dc.description.numberofpages11en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Martin, D-
dc.contributor.wosstandardWOS:Rojo, AI-
dc.contributor.wosstandardWOS:Salinas, M-
dc.contributor.wosstandardWOS:Diaz, R-
dc.contributor.wosstandardWOS:Gallardo, G-
dc.contributor.wosstandardWOS:Alam, J-
dc.contributor.wosstandardWOS:de Galarreta, CMR-
dc.contributor.wosstandardWOS:Cuadrado, A-
dc.date.coverdateMarzo 2004en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.jcr6,355-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptGIR Didáctica, Aprendizaje y Motivación en Contextos Específicos-
crisitem.author.deptDepartamento de Didácticas Específicas-
crisitem.author.deptGIR Biomaterials and Biomechanics Research Group-
crisitem.author.deptDepartamento de Ingeniería Mecánica-
crisitem.author.orcid0000-0002-1516-1750-
crisitem.author.orcid0000-0002-8599-781X-
crisitem.author.parentorgDepartamento de Educación-
crisitem.author.parentorgDepartamento de Ingeniería Mecánica-
crisitem.author.fullNameGallardo Campos, Germán-
crisitem.author.fullNameRuiz De Galarreta Hernandez,C. Manuel-
crisitem.author.fullNameCuadrado Hernández, Alberto Javier-
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