Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/8707
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dc.contributor.authorNobles, Murieles
dc.contributor.authorMontaigne, Davides
dc.contributor.authorSebastian, Soniaes
dc.contributor.authorBirnbaumer, Lutzes
dc.contributor.authorTinker, Andrewes
dc.date.accessioned2019-09-10T18:01:18Z-
dc.date.available2019-09-10T18:01:18Z-
dc.date.issued2018-
dc.identifier.citationNobles M, Montaigne D, Sebastian S, Birnbaumer L, Tinker A. Differential effects of inhibitory G protein isoforms on G protein-gated inwardly rectifying K+ currents in adult murine atria [en línea]. American Journal of Physiology-Cell Physiology. 2018;314(5):C616-C626. doi:10.1152/ajpcell.00271.2016 Disponible en: https://repositorio.uca.edu.ar/handle/123456789/8707es
dc.identifier.issn0363-6143-
dc.identifier.issn1522-1563 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/8707-
dc.description.abstractAbstract: G protein-gated inwardly rectifying K+ (GIRK) channels are the major inwardly rectifying K+ currents in cardiac atrial myocytes and an important determinant of atrial electrophysiology. Inhibitory G protein α-subunits can both mediate activation via acetylcholine but can also suppress basal currents in the absence of agonist. We studied this phenomenon using whole cell patch clamping in murine atria from mice with global genetic deletion of Gαi2, combined deletion of Gαi1/Gαi3, and littermate controls. We found that mice with deletion of Gαi2 had increased basal and agonist-activated currents, particularly in the right atria while in contrast those with Gαi1/Gαi3 deletion had reduced currents. Mice with global genetic deletion of Gαi2 had decreased action potential duration. Tissue preparations of the left atria studied with a multielectrode array from Gαi2 knockout mice showed a shorter effective refractory period, with no change in conduction velocity, than littermate controls. Transcriptional studies revealed increased expression of GIRK channel subunit genes in Gαi2 knockout mice. Thus different G protein isoforms have differential effects on GIRK channel behavior and paradoxically Gαi2 act to increase basal and agonist-activated GIRK currents. Deletion of Gαi2 is potentially proarrhythmic in the atria.es
dc.formatapplication/pdfes
dc.language.isoenges
dc.publisherAmerican Physiological Societyes
dc.rightsAcceso Abierto*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.sourceAmerican Journal of Physiology-Cell Physiology. 2018;314(5):C616-C626es
dc.subjectPOTASIOes
dc.subjectRITMO CARDIACOes
dc.subjectARRITMIAes
dc.subjectCORAZONes
dc.subjectFIBRILACION AURICULARes
dc.titleDifferential effects of inhibitory G protein isoforms on G protein-gated inwardly rectifying K+ currents in adult murine atriaes
dc.typeArtículoes
dc.identifier.doi10.1152/ajpcell.00271.2016-
dc.identifier.pmid29342363-
dc.contributor.orcid0000-0002-7654-2565-
uca.disciplinaMEDICINA-
uca.issnrd1es
uca.affiliationFil: Nobles, Muriel. Barts and the London School of Medicine and Dentistry. William Harvey Research Institute. The Heart Centre; Reino Unidoes
uca.affiliationFil: Montaigne, David. Centre Hospitalier Régional Universitaire de Lille; Franciaes
uca.affiliationFil: Montaigne, David. Université Lille 2; Franciaes
uca.affiliationFil: Sebastian, Sonia. Barts and the London School of Medicine and Dentistry. William Harvey Research Institute. The Heart Centre; Reino Unidoes
uca.affiliationFil: Sebastian, Sonia. Institut National de la Santé et de la Recherche Médicale; Franciaes
uca.affiliationFil: Sebastian, Sonia. European Genomic Institute for Diabetes; Franciaes
uca.affiliationFil: Sebastian, Sonia. Institut Pasteur de Lille; Franciaes
uca.affiliationFil: Birnbaumer, Lutz. Research Triangle Park. National Institute of Environmental Health Sciences. Division of Intramural Research; Estados Unidoses
uca.affiliationFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instituto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Tinker, Andrew. Barts and the London School of Medicine and Dentistry. William Harvey Research Institute. The Heart Centre; Reino Unidoes
uca.versionpublishedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Función y Farmacología de Canales Iónicos-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.orcid0000-0002-0775-8661-
crisitem.author.parentorgFacultad de Ciencias Médicas-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
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