LYP 可调节 T 细胞中的 SLP76 和其他适配蛋白。

IF 4.3 2区生物学 Q1 BIOLOGY Biological Research Pub Date : 2024-09-28 DOI:10.1186/s40659-024-00536-8

Virginia Ruiz-Martín, Tamara Marcos, José María de Pereda, Mariano Sánchez-Crespo, Miguel Angel de la Fuente, Yolanda Bayón, Andrés Alonso

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引用次数: 0

摘要

背景：LYP酪氨酸磷酸酶存在一个 SNP（1858C > T），会增加罹患 I 型糖尿病和关节炎等自身免疫性疾病的风险。目前仍不清楚该 SNP 如何影响 LYP 的功能并促进这些疾病的发生。有关 LYP 底物的信息稀缺是导致人们对 LYP 功能了解甚少的部分原因：在这项研究中，我们在 T 淋巴细胞中发现了几个适配蛋白是 LYP 的潜在底物，包括 FYB、SLP-76、HS-1、Vav、SKAP1 和 SKAP2。我们还发现，在 TCR 参与时，LYP 与 SLP76 共同定位在微集群中：这些数据表明，LYP 可在 TCR 接合时通过使 FYB、SLP-76、HS-1、Vav、SKAP1 和 SKAP2 等几种适配蛋白去磷酸化来调节 T 细胞的活化。

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LYP regulates SLP76 and other adaptor proteins in T cells.

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.

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来源期刊

Biological Research 生物-生物学

CiteScore

10.10

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Biological Research is an open access, peer-reviewed journal that encompasses diverse fields of experimental biology, such as biochemistry, bioinformatics, biotechnology, cell biology, cancer, chemical biology, developmental biology, evolutionary biology, genetics, genomics, immunology, marine biology, microbiology, molecular biology, neuroscience, plant biology, physiology, stem cell research, structural biology and systems biology.