Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/48259
DC FieldValueLanguage
dc.contributor.authorRico-Bautista, Elizabethen_US
dc.contributor.authorNegrín-Martínez, Ciroen_US
dc.contributor.authorNovoa Mogollón, Franciscoen_US
dc.contributor.authorFernández-Perez, Leandroen_US
dc.contributor.authorFlores-Morales, Amilcaren_US
dc.date.accessioned2018-11-23T20:13:21Z-
dc.date.available2018-11-23T20:13:21Z-
dc.date.issued2004en_US
dc.identifier.issn0014-4827en_US
dc.identifier.urihttp://hdl.handle.net/10553/48259-
dc.description.abstractTransient activation of the signal transducers and activators of transcription (STAT) proteins in response to growth hormone (GH) and other type II cytokines plays a pivotal role on specific gene transcription. The negative regulation of STATs seems to be exerted at the GH receptor (GHR)/Janus Kinase (JAK) complex and involves two main mechanisms: (1) the GH-induced ubiquitination/internalization of GHR and (2) the action of SOCS proteins. Since GH regulates cellular cytoskeleton with potential implications in GH signaling, we investigated the effects of actin cytoskeleton disruption on the kinetics of GH-activated GHR/Janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5) signaling pathway. Disruption of the actin-based cytoskeleton with cytochalasin D (CytoD) did not affect the rapid GH induction of JAK2 and STAT5 activities. However, pretreatment of BRL-4 cells with CytoD prolonged both, JAK2/STAT5 tyrosine phosphorylation and STAT5 DNA binding activity, for at least 2 h. Our results demonstrated that the synthesis of the several SOCS proteins (SOCS-1, -2, and -3) was not affected by treatment of the cells with CytoD. On the other hand, the inhibitory actions of SOCS 1, 2, and -3 on GH-induced STAT5 reporter activity were partially blocked by disruption of the cytoskeleton. Disassembly of the actin filaments by CytoD is accompanied by accumulation of ubiquitinated forms of GHR but it does not affect GHR internalization. We conclude that the integrity of the actin cytoskeleton network plays an essential role in the negative regulation of GHR/JAK2/STAT5 signaling pathway by facilitating the GHR ubiquitination/degradation through mechanisms acting downstream SOCS.en_US
dc.languageengen_US
dc.relation.ispartofExperimental cell researchen_US
dc.sourceExperimental Cell Research[ISSN 0014-4827],v. 294, p. 269-280en_US
dc.subject32 Ciencias médicasen_US
dc.subject3201 Ciencias clínicasen_US
dc.subject.otherTyrosyl Phosphorylationen_US
dc.subject.otherEndoplasmic-Reticulumen_US
dc.subject.otherCytokine Signaling-2en_US
dc.subject.otherProtein-Synthesisen_US
dc.subject.otherEpithelial-Cellsen_US
dc.subject.otherGene-Expressionen_US
dc.subject.otherReceptoren_US
dc.subject.otherEndocytosisen_US
dc.subject.otherSystemen_US
dc.subject.otherJak2en_US
dc.titleDownregulation of the growth hormone-induced Janus kinase 2/signal transducer and activator of transcription 5 signaling pathway requires an intact actin cytoskeletonen_US
dc.typeinfo:eu-repo/semantics/Articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1016/j.yexcr.2003.11.017en_US
dc.identifier.scopus1242339600-
dc.identifier.isi000220028300026-
dc.contributor.authorscopusid6508139241-
dc.contributor.authorscopusid6505525090-
dc.contributor.authorscopusid12786120600-
dc.contributor.authorscopusid6506777525-
dc.contributor.authorscopusid57203543352-
dc.description.lastpage280en_US
dc.description.firstpage269en_US
dc.relation.volume294en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.contributor.daisngid3599226-
dc.contributor.daisngid11865715-
dc.contributor.daisngid6408279-
dc.contributor.daisngid795544-
dc.contributor.daisngid617657-
dc.description.numberofpages12en_US
dc.utils.revisionen_US
dc.contributor.wosstandardWOS:Rico-Bautista, E-
dc.contributor.wosstandardWOS:Negrin-Martinez, C-
dc.contributor.wosstandardWOS:Novoa-Mogollon, J-
dc.contributor.wosstandardWOS:Fernandez-Perez, L-
dc.contributor.wosstandardWOS:Flores-Morales, A-
dc.date.coverdateMarzo 2004en_US
dc.identifier.ulpgcen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.jcr4,007-
dc.description.jcrqQ1-
dc.description.scieSCIE-
item.grantfulltextnone-
item.fulltextSin texto completo-
crisitem.author.deptGIR Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.orcid0000-0003-3629-8120-
crisitem.author.orcid0000-0001-7802-465X-
crisitem.author.orcid0000-0002-0828-8921-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameNovoa Mogollón, Francisco-
crisitem.author.fullNameFernández Pérez, Leandro Fco-
crisitem.author.fullNameFlores Morales, Amilcar-
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