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dc.creatorNajimi, Mustapha
dc.creatorSouaze, Frédérique
dc.creatorMéndez, Milagros
dc.creatorHermans, Emmanuel
dc.creatorBerbar, Tsouria
dc.creatorRostene, William
dc.creatorForgez, Patricia
dc.date.accessioned2017-06-30T03:50:47Z
dc.date.available2017-06-30T03:50:47Z
dc.date.issued1998es_ES
dc.identifier2320es_ES
dc.identifier.issn0021-9258es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/6965
dc.identifier.urihttps://doi.org/10.1074/jbc.273.34.21634es_ES
dc.language.isoenges_ES
dc.publisherAmer Soc Biochemistry Molecular Biology INC, 9650 Rockville Pike, Bethesda, MD 20814 USAes_ES
dc.relation273 (34) 21634-21641 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleActivation of receptor gene transcription is required to maintain cell sensitization after agonist exposure. Study on neurotensin receptores_ES
dc.typearticlees_ES
dc.contributor.affiliationHop St Antoine, INSERM U339, 184 Rue Faubourg St Antoine, F-75012 Paris, Francees_ES
dc.relation.jnabreviadoJ. BIOL CHEMes_ES
dc.relation.journalThe Journal of Biological Chemistryes_ES
dc.identifier.placeBethesdaes_ES
dc.date.published1998es_ES
dc.identifier.eissn1083-351Xes_ES
dc.identifier.doi10.1074/jbc.273.34.21634es_ES
dc.description.monthAgoes_ES
dc.description.abstractotrodiomaNeurotensin (NT) acts through specific G protein-coupled receptors to induce effects in the central nervous system and periphery. In this study we have shown that in the human neuroblastoma cell Line CHP 212, an NT agonist, JMV 449, induced high affinity neurotensin receptor (NTR) gene activation. I-125-NT binding of cells challenged with JMV 449 rapidly decreased then reappeared and subsequently stabilized at 50% of the control values after 48 h of agonist exposure. These receptors, which reappeared at the cell surface, are as active as those found in control cells as demonstrated by Ca2+ mobilization. Furthermore, the tyrosine hydroxylase (TH) gene, a known NT target gene, remained activated after prolonged NT agonist exposure in this cell line. In the murine neuroblastoma cell line, N1E-115, NT did not stimulate NTR gene activation but induced NTR mRNA destabilization after long term agonist exposure. In this cell line, NT binding dropped to 15% of control values and remained at this value after agonist treatment. The TH expression, which was originally activated upon NT agonist exposure, decreased to control values after prolonged agonist exposure. These observations combined with the data obtained from a complementary study with HT-29 cells (Souaze, F., Rostene, W., and Forgez, P. (1997) J. Biol. Chem. 272, 10087-10094) revealed the crucial role of agonist-induced receptor gene transcription in the maintenance of cell sensitivity. A model for G protein-coupled receptor regulation induced by prolong and intense agonist stimulation is proposed.es_ES
dc.subject.kwReceptores de la transcripción génicaes_ES
dc.subject.kwSensibilización celulares_ES
dc.subject.kwExposición agonistaes_ES
dc.subject.kwNeurotensinaes_ES
dc.subject.koReceptor Gene Transcriptiones_ES
dc.subject.koCell Sensitizationes_ES
dc.subject.koAgonist Exposurees_ES
dc.subject.koNeurotensines_ES


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