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dc.contributor.authorBlas-Rus, Noelia-
dc.contributor.authorAlarcón, Balbino-
dc.contributor.authorSánchez-Madrid, Francisco-
dc.date.accessioned2017-05-29T07:50:54Z-
dc.date.available2017-05-29T07:50:54Z-
dc.date.issued2016-04-19-
dc.identifierdoi: 10.1038/ncomms11389-
dc.identifierissn: 2041-1723-
dc.identifier.citationNature Communications 7: 11389 (2016)-
dc.identifier.urihttp://hdl.handle.net/10261/150537-
dc.description.abstractAurora A is a serine/threonine kinase that contributes to the progression of mitosis by inducing microtubule nucleation. Here we have identified an unexpected role for Aurora A kinase in antigen-driven T-cell activation. We find that Aurora A is phosphorylated at the immunological synapse (IS) during TCR-driven cell contact. Inhibition of Aurora A with pharmacological agents or genetic deletion in human or mouse T cells severely disrupts the dynamics of microtubules and CD3¿-bearing vesicles at the IS. The absence of Aurora A activity also impairs the activation of early signalling molecules downstream of the TCR and the expression of IL-2, CD25 and CD69. Aurora A inhibition causes delocalized clustering of Lck at the IS and decreases phosphorylation levels of tyrosine kinase Lck, thus indicating Aurora A is required for maintaining Lck active. These findings implicate Aurora A in the propagation of the TCR activation signal.-
dc.description.sponsorshipSpanish Ministry of Economy and Competitiveness, NDISNET-S2011/BMD-2332 from the Comunidad de Madrid ERC-2011-AdG 294340-GENTRIS and ERC-2013-AdG 334763-NOVARIPP. Red Cardiovascular RD 12-0042-0056 from Instituto Salud Carlos III (ISCIII). The Centro Nacional de Investigaciones Cardiovasculares (CNIC, Spain) is supported by the Spanish Ministry of Science and Innovation, and the Pro-CNIC Foundation-
dc.publisherNature Publishing Group-
dc.relation.isversionofPublisher's version-
dc.rightsopenAccess-
dc.titleAurora a drives early signalling and vesicle dynamics during T-cell activation-
dc.typeartículo-
dc.identifier.doi10.1038/ncomms11389-
dc.date.updated2017-05-29T07:50:54Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.rights.licensehttps://creativecommons.org/licenses/by/4.0/-
dc.contributor.funderFundación Pro CNIC-
dc.contributor.funderMinisterio de Ciencia e Innovación (España)-
dc.contributor.funderCentro Nacional de Investigaciones Cardiovasculares (España)-
dc.contributor.funderInstituto de Salud Carlos III-
dc.contributor.funderComunidad de Madrid-
dc.contributor.funderMinisterio de Economía y Competitividad (España)-
dc.relation.csic-
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004837es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100005884es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100004587es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/100012818es_ES
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