<?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>2026-06-14T03:37:46Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/7212" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/7212</identifier><datestamp>2024-11-28T16:01:40Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>com_20.500.12105_2173</setSpec><setSpec>com_20.500.12105_15322</setSpec><setSpec>col_20.500.12105_19605</setSpec><setSpec>col_20.500.12105_19597</setSpec><setSpec>col_20.500.12105_16938</setSpec><setSpec>col_20.500.12105_16980</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">Bustos-Morán, Eugenio</subfield>
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      <subfield code="a">Blas-Rus, Noelia</subfield>
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      <subfield code="a">Alcaraz-Serna, Ana</subfield>
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      <subfield code="a">Iborra, Salvador</subfield>
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      <subfield code="a">González-Martínez, José</subfield>
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      <subfield code="a">Malumbres Martinez, Marcos</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 whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4+ T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8+ T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8+ T cells. This finding was similarly proven for both mice and human CD8+ CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as granzyme B or perforin1. Finally, we have found that Aurora A is necessary for CD8+ T cell-mediated antiviral response, in an in vivo model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.</subfield>
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      <subfield code="a">Sci Rep. 2019; 9(1):2211</subfield>
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      <subfield code="a">10.1038/s41598-019-38647-y</subfield>
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      <subfield code="a">30778113</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/7212</subfield>
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      <subfield code="a">Aurora A controls CD8+ T cell cytotoxic activity and antiviral response</subfield>
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