<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-14T03:42:48Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/5241" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/5241</identifier><datestamp>2025-02-27T11:24:52Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>com_20.500.12105_2173</setSpec><setSpec>col_20.500.12105_19605</setSpec><setSpec>col_20.500.12105_19597</setSpec><setSpec>col_20.500.12105_19607</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Blas-Rus, Noelia</subfield>
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      <subfield code="a">Bustos-Moran, Eugenio</subfield>
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      <subfield code="a">Perez de Castro, Ignacio</subfield>
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      <subfield code="a">de Carcer Diez, Guillermo</subfield>
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      <subfield code="a">Borroto, Aldo</subfield>
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      <subfield code="a">Camafeita, Emilio</subfield>
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      <subfield code="a">Jorge, Inmaculada</subfield>
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      <subfield code="a">Vazquez, Jesus</subfield>
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      <subfield code="a">Alarcón, Balbino</subfield>
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      <subfield code="a">Martin-Cofreces, Noa B.</subfield>
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      <subfield code="a">Sanchez-Madrid, Francisco</subfield>
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      <subfield code="a">Aurora 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 CD3z-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.</subfield>
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      <subfield code="a">Nat Commun. 2016; 7:11389</subfield>
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      <subfield code="a">10.1038/ncomms11389</subfield>
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      <subfield code="a">Nature Communications</subfield>
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      <subfield code="a">27091106</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/5241</subfield>
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      <subfield code="a">IMMUNOLOGICAL SYNAPSE</subfield>
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      <subfield code="a">IMMUNE SYNAPSE</subfield>
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      <subfield code="a">TIRF MICROSCOPY</subfield>
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      <subfield code="a">CENTROSOME MATURATION</subfield>
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      <subfield code="a">ANTIGEN RECEPTOR</subfield>
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      <subfield code="a">TYROSINE KINASE</subfield>
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      <subfield code="a">A KINASE</subfield>
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      <subfield code="a">Aurora A drives early signalling and vesicle dynamics during T-cell activation</subfield>
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