<?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>2026-04-04T02:27:20Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:2445/186239" metadataPrefix="marc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:2445/186239</identifier><datestamp>2025-12-16T20:06:03Z</datestamp><setSpec>com_2072_1057</setSpec><setSpec>col_2072_478781</setSpec><setSpec>col_2072_478917</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Vallejo-Gracia, Albert</subfield>
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      <subfield code="a">Hajdú, Péter</subfield>
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      <subfield code="a">Felipe Campo, Antonio</subfield>
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      <subfield code="a">The voltage-dependent potassium channel Kv1.3 plays essential roles in the immune system, participating in leukocyte activation, proliferation and apoptosis. The regulatory subunit KCNE4 acts as an ancillary peptide of Kv1.3, modulates K+ currents and controls channel abundance at the cell surface. KCNE4-dependent regulation of the oligomeric complex fne-tunes the physiological role of Kv1.3. Thus, KCNE4 is crucial for Ca2+-dependent Kv1.3-related leukocyte functions. To better understand the role of KCNE4 in the regulation of the immune system, we manipulated its expression in various leukocyte cell lines. Jurkat T lymphocytes exhibit low KCNE4 levels, whereas CY15 dendritic cells, a model of professional antigen-presenting cells, robustly express KCNE4. When the cellular KCNE4 abundance was increased in T cells, the interaction between KCNE4 and Kv1.3 afected important T cell physiological features, such as channel rearrangement in the immunological synapse, cell growth, apoptosis and activation, as indicated by decreased IL-2 production. Conversely, ablation of KCNE4 in dendritic cells augmented proliferation. Furthermore, the LPS-dependent activation of CY15 cells, which induced Kv1.3 but not KCNE4, increased the Kv1.3-KCNE4 ratio and increased the expression of free Kv1.3 without KCNE4 interaction. Our results demonstrate that KCNE4 is a pivotal regulator of the Kv1.3 channelosome, which fne-tunes immune system physiology by modulating Kv1.3-associated leukocyte functions.</subfield>
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      <subfield code="a">Sistema immunitari</subfield>
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      <subfield code="a">Leucòcits</subfield>
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      <subfield code="a">Cèl·lules T</subfield>
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      <subfield code="a">Potassium channels</subfield>
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      <subfield code="a">Immune system</subfield>
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      <subfield code="a">KCNE4-dependent functional consequences of Kv1.3-related leukocyte physiology.</subfield>
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