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dc.contributor.authorPérez García, María Teresa 
dc.contributor.authorLópez López, José Ramón 
dc.date.accessioned2020-12-28T12:48:36Z
dc.date.available2020-12-28T12:48:36Z
dc.date.issued2000
dc.identifier.citationCirculation Research, 2000, vol. 86, n. 5. p. 490-491es
dc.identifier.issn1524-4571es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/44606
dc.descriptionProducción Científicaes
dc.description.abstractThis report represents a relevant contribution to the study of oxygen sensing for two main reasons. First, it shows an approach adequate for identification of a putative O2-sensitive K+ channel, by moving from the modulation by hypoxia of a recombinant channel back to its physiological context, the role of this channel in the response to low Po2 of the native cells. Second, it demonstrates that hypoxic inhibition of the recombinant Kv3.1 channels is retained in excised membrane patches, pointing to a membrane-delimited mechanism as the origin of hypoxic responses. The importance of this latter finding deserves additional comment.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherAmerican Heart Associationes
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.subject.classificationPotassium channelses
dc.subject.classificationCanales de potasioes
dc.subject.classificationOxygen sensinges
dc.subject.classificationDetección de oxígenoes
dc.titleAre Kv channels the essence of O2 sensing?es
dc.typeinfo:eu-repo/semantics/articlees
dc.rights.holder© 2000 American Heart Associationes
dc.identifier.doi10.1161/01.RES.86.5.490es
dc.relation.publisherversionhttps://www.ahajournals.org/doi/10.1161/01.RES.86.5.490es
dc.peerreviewedSIes
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersiones


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