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<mods:namePart>Ruiz Martín, Virginia</mods:namePart>
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<mods:namePart>de Pereda, José María</mods:namePart>
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<mods:namePart>Fuente García, Miguel Ángel de la</mods:namePart>
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<mods:namePart>Bayón Prieto, Yolanda</mods:namePart>
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<mods:namePart>Alonso, Andrés</mods:namePart>
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<mods:identifier type="citation">Biological Research volume 57, Article number: 69 (2024)</mods:identifier>
<mods:identifier type="uri">https://uvadoc.uva.es/handle/10324/73882</mods:identifier>
<mods:identifier type="doi">10.1186/s40659-024-00536-8</mods:identifier>
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<mods:identifier type="publicationtitle">LYP regulates SLP76 and other adaptor proteins in T cells</mods:identifier>
<mods:identifier type="publicationvolume">volume 57</mods:identifier>
<mods:abstract>Background&#xd;
&#xd;
The LYP tyrosine phosphatase presents a SNP (1858C > T) that increases the risk of developing autoimmune diseases such as type I diabetes and arthritis. It remains unclear how this SNP affects LYP function and promotes the development of these diseases. The scarce information about LYP substrates is in part responsible for the poor understanding of LYP function.&#xd;
Results&#xd;
&#xd;
In this study, we identify in T lymphocytes several adaptor proteins as potential substrates targeted by LYP, including FYB, SLP-76, HS-1, Vav, SKAP1 and SKAP2. We also show that LYP co-localizes with SLP76 in microclusters, upon TCR engagement.&#xd;
Conclusions&#xd;
&#xd;
These data indicate that LYP may modulate T cell activation by dephosphorylating several adaptor proteins, such as FYB, SLP-76, HS-1, Vav, SKAP1 and SKAP2 upon TCR engagement.</mods:abstract>
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<mods:accessCondition type="useAndReproduction">Attribution-NonCommercial-NoDerivatives 4.0 Internacional</mods:accessCondition>
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<mods:topic>Biomedicina</mods:topic>
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<mods:titleInfo>
<mods:title>LYP regulates SLP76 and other adaptor proteins in T cells</mods:title>
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