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Insulin-mediated upregulation of T-type Ca2+ currents in GH3 cells is mediated by increased endosomal recycling and incorporation of surface membrane Cav3.1 channels

dc.creatorToledo, Alicia
dc.creatorSandoval, Alejandro
dc.creatorGonzález-Ramírez, Ricardo
dc.creatorÁvila, Traudy
dc.creatorAlmanza, Angélica
dc.creatorMonjaraz, Eduardo
dc.creatorGomora, Juan Carlos
dc.creatorPiedras-Rentería, Erika S.
dc.creatorFelix, Ricardo
dc.date.accessioned2017-06-29T03:54:04Z
dc.date.available2017-06-29T03:54:04Z
dc.date.issued2012es_ES
dc.identifier2769es_ES
dc.identifier.issn0143-4160es_ES
dc.identifier.urihttps://doi.org/10.1016/j.ceca.2012.06.005es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4618
dc.description.abstractes_ES
dc.language.isoenges_ES
dc.publisher[Edinburgh, New York] Churchill Livingston  Amsterdam : Elsevieres_ES
dc.relation52 (5) 377-387 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.subject.meshAnimalses_ES
dc.subject.meshBrefeldin A/pharmacologyes_ES
dc.subject.meshCalcium Channels, T-Type/geneticses_ES
dc.subject.meshCalcium Channels, T-Type/metabolismes_ES
dc.subject.meshCell Membrane Permeability/drug effectses_ES
dc.subject.meshEndosomes/drug effectses_ES
dc.subject.meshEndosomes/metabolismes_ES
dc.subject.meshGene Expression Regulation/drug effectses_ES
dc.subject.meshGene Expression Regulation/geneticses_ES
dc.subject.meshHEK293 Cellses_ES
dc.subject.meshHumanses_ES
dc.subject.meshInsulin/metabolismes_ES
dc.subject.meshMonomeric GTP-Binding Proteins/geneticses_ES
dc.subject.meshMutation/geneticses_ES
dc.subject.meshPatch-Clamp Techniqueses_ES
dc.subject.meshPituitary Gland/cytologyes_ES
dc.subject.meshPituitary Gland/metabolismes_ES
dc.subject.meshRatses_ES
dc.subject.meshTranscriptional Activation/drug effectses_ES
dc.subject.meshTranscriptional Activation/geneticses_ES
dc.subject.meshrab GTP-Binding Proteins/geneticses_ES
dc.titleInsulin-mediated upregulation of T-type Ca2+ currents in GH3 cells is mediated by increased endosomal recycling and incorporation of surface membrane Cav3.1 channelses_ES
dc.title.alternativees_ES
dc.typeartículoes_ES
dc.contributor.affiliationDepartment of Cell Biology, Center for Research and Advanced Studies of the National Polytechnic Institute (Cinvestav-IPN), Mexico City, Mexicoes_ES
dc.contributor.emailrfelix@cell.cinvestav.mxes_ES
dc.relation.jnabreviadoCELL CALCIUMes_ES
dc.relation.journalCell Calciumes_ES
dc.identifier.placePaíses Bajoses_ES
dc.date.published2012es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1532-1991es_ES
dc.identifier.doi10.1016/j.ceca.2012.06.005es_ES
dc.description.monthNoves_ES
dc.description.abstractotrodiomaGrowth factors and hormones have both short- and long-term regulatory effects on the functional expression of voltage gated Ca2+ (CaV) channels. In particular, it has been reported that chronic treatment with insulin upregulates T-type channel membrane expression, leading to an increase in current density in clonal pituitary GH3 cells. Though this regulatory action may result from alterations in gene expression, recent studies have demonstrated also that endosomal trafficking provides a mechanism for dynamic changes in CaV channel membrane density. Therefore, in the present work we sought to determine whether the actions of insulin on T-type channel functional expression are mediated by transcriptional and/or post-transcriptional mechanisms. Using real-time RT-PCR and semi-quantitative western blot we found no changes after treatmentin the transcript and protein levels of Cav3.1,the T-type channel isoform preferentially expressed in the GH3 cells. Consistent with this, transcriptional studies using a luciferase reporter assay suggested that insulin treatment does not affect the Cav3.1 promoter activity. In contrast, patch-clamp recordings on HEK-293 cells stably expressing Cav3.1 channels showed a significantincrease in current density after treatment, suggesting that the effects of insulin may require post-transcriptional regulation. In line with this, disruption of the endosomal recycling pathway using Brefeldin A and a dominant negative mutant of the small GTPase Rab11a prevented the stimulatory effects of insulin on Cav3.1 channels in HEK-293 cells. These results may help explain the effects of insulin on T-type channels and contribute to our understanding of how endosomal recycling impacts the functional expression of CaV channels.es_ES
dc.subject.meshmes_ES
dc.subject.kwes_ES
dc.subject.koCa2+ channelses_ES
dc.subject.koInsulines_ES
dc.subject.koCav3.1 channelses_ES
dc.subject.koRab11es_ES
dc.subject.koEndosome recyclinges_ES


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