Identificador persistente para citar o vincular este elemento: http://hdl.handle.net/10553/54586
Campo DC Valoridioma
dc.contributor.authorRuiz-García, Almudenaen_US
dc.contributor.authorMonsalve, Evaen_US
dc.contributor.authorNovellasdemunt, Lauraen_US
dc.contributor.authorNavarro-Sabaté, Áureaen_US
dc.contributor.authorManzano, Annaen_US
dc.contributor.authorRivero, Samuelen_US
dc.contributor.authorCastrillo Viguera, Antonio Jesúsen_US
dc.contributor.authorCasado, Martaen_US
dc.contributor.authorLaborda, Jorgeen_US
dc.contributor.authorBartrons, Ramónen_US
dc.contributor.authorDíaz-Guerra, María José M.en_US
dc.date.accessioned2019-02-18T11:47:00Z-
dc.date.available2019-02-18T11:47:00Z-
dc.date.issued2011en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10553/54586-
dc.description.abstractMacrophages activated through Toll receptor triggering increase the expression of the A(2A) and A(2B) adenosine receptors. In this study, we show that adenosine receptor activation enhances LPS-induced pfkfb3 expression, resulting in an increase of the key glycolytic allosteric regulator fructose 2,6-bisphosphate and the glycolytic flux. Using shRNA and differential expression of A(2A) and A(2B) receptors, we demonstrate that the A(2A) receptor mediates, in part, the induction of pfkfb3 by LPS, whereas the A(2B) receptor, with lower adenosine affinity, cooperates when high adenosine levels are present. pfkfb3 promoter sequence deletion analysis, site-directed mutagenesis, and inhibition by shRNAs demonstrated that HIF1 alpha is a key transcription factor driving pfkfb3 expression following macrophage activation by LPS, whereas synergic induction of pfkfb3 expression observed with the A(2) receptor agonists seems to depend on Sp1 activity. Furthermore, levels of phospho-AMP kinase also increase, arguing for increased PFKFB3 activity by phosphorylation in long term LPS-activated macrophages. Taken together, our results show that, in macrophages, endogenously generated adenosine cooperates with bacterial components to increase PFKFB3 isozyme activity, resulting in greater fructose 2,6-bisphosphate accumulation. This process enhances the glycolytic flux and favors ATP generation helping to develop and maintain the long term defensive and reparative functions of the macrophages.en_US
dc.languagespaen_US
dc.publisher0021-9258
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.sourceJournal of Biological Chemistry[ISSN 0021-9258],v. 286, p. 19247-19258en_US
dc.subject.otherNf-Kappa-B
dc.subject.otherHypoxia-Inducible Factor-1-Alpha
dc.subject.otherActivated Protein-Kinase
dc.subject.otherTumor-Necrosis-Factor
dc.subject.otherUp-Regulation
dc.subject.otherTranscription Factor
dc.subject.otherFactor Induction
dc.subject.otherImmune-Response
dc.subject.otherNitric-Oxide
dc.subject.otherC/Ebp-Delta
dc.titleCooperation of adenosine with macrophage toll-4 receptor agonists leads to increased glycolytic flux through the enhanced expression of PFKFB3 geneen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1074/jbc.M110.190298en_US
dc.identifier.scopus79957587060-
dc.identifier.isi000291027700007-
dc.contributor.authorscopusid35077961800-
dc.contributor.authorscopusid16039649600-
dc.contributor.authorscopusid38661458800-
dc.contributor.authorscopusid6507020659-
dc.contributor.authorscopusid7003973260-
dc.contributor.authorscopusid16040660200-
dc.contributor.authorscopusid55445301000-
dc.contributor.authorscopusid7103101615-
dc.contributor.authorscopusid7003504698-
dc.contributor.authorscopusid7007151916-
dc.contributor.authorscopusid7004245830-
dc.description.lastpage19258en_US
dc.description.firstpage19247en_US
dc.relation.volume286en_US
dc.type2Artículoen_US
dc.contributor.daisngid5413547-
dc.contributor.daisngid2280332-
dc.contributor.daisngid4768916-
dc.contributor.daisngid1750898-
dc.contributor.daisngid1241005-
dc.contributor.daisngid4837467-
dc.contributor.daisngid225640-
dc.contributor.daisngid466535-
dc.contributor.daisngid408952-
dc.contributor.daisngid153393-
dc.contributor.daisngid1524431-
dc.contributor.wosstandardWOS:Ruiz-Garcia, A-
dc.contributor.wosstandardWOS:Monsalve, E-
dc.contributor.wosstandardWOS:Novellasdemunt, L-
dc.contributor.wosstandardWOS:Navarro-Sabate, A-
dc.contributor.wosstandardWOS:Manzano, A-
dc.contributor.wosstandardWOS:Rivero, S-
dc.contributor.wosstandardWOS:Castrillo, A-
dc.contributor.wosstandardWOS:Casado, M-
dc.contributor.wosstandardWOS:Laborda, J-
dc.contributor.wosstandardWOS:Bartrons, R-
dc.contributor.wosstandardWOS:Diaz-Guerra, MJM-
dc.date.coverdateJunio 2011en_US
dc.identifier.ulpgces
dc.description.sjr3,495
dc.description.jcr4,773
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextSin texto completo-
item.grantfulltextnone-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.orcid0000-0002-2057-2159-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameCastrillo Viguera,Antonio Jesús-
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