2026-04-26T20:24:45Zhttps://uvadoc.uva.es/oai/request

oai:uvadoc.uva.es:10324/738822025-03-26T16:41:30Zcom_10324_1134com_10324_931com_10324_894col_10324_1213

Ruiz Martín, Virginia Marcos, Tamara de Pereda, José María Sánchez Crespo, Mariano Fuente García, Miguel Ángel de la Bayón Prieto, Yolanda Alonso, Andrés 2024 Producción Científica Background 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. Results 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. Conclusions 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. application/pdf https://uvadoc.uva.es/handle/10324/73882 eng BioMed Central (BMC)-Part of Springer Nature Biomedicina 24 Ciencias de la Vida LYP regulates SLP76 and other adaptor proteins in T cells info:eu-repo/semantics/article TEXT UVaDOC. Repositorio Documental de la Universidad de Valladolid Hispana