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Recruitment of tyrosine phosphatase HCP by the killer cell inhibitor receptor.
Immunity ( IF 25.5 ) Pub Date : 1996-01-01 , DOI: 10.1016/s1074-7613(00)80300-3
D N Burshtyn 1 , A M Scharenberg , N Wagtmann , S Rajagopalan , K Berrada , T Yi , J P Kinet , E O Long
Affiliation  

Cytolysis of target cells by natural killer (NK) cells and by some cytotoxic T cells occurs unless prevented by inhibitory receptors that recognize MHC class I on target cells. Human NK cells express a p58 inhibitory receptor specific for HLA-C. We report association of the tyrosine phosphatase HCP with the p58 receptor in NK cells. HCP association was dependent on tyrosine phosphorylation of p58. Phosphotyrosyl peptides corresponding to the p58 tail bound and activated HCP in vitro. Furthermore, introduction of an inactive mutant HCP into an NK cell line prevented the p58-mediated inhibition of target cell lysis. These data imply that the inhibitory function of p58 is dependent on its tyrosine phosphorylation and on recruitment and activation of HCP.

中文翻译:


杀伤细胞抑制剂受体招募酪氨酸磷酸酶 HCP。



除非被识别靶细胞上 MHC I 类的抑制性受体阻止,否则自然杀伤 (NK) 细胞和某些细胞毒性 T 细胞会对靶细胞进行细胞溶解。人类 NK 细胞表达 HLA-C 特异性的 p58 抑制性受体。我们报告了 NK 细胞中酪氨酸磷酸酶 HCP 与 p58 受体的关联。 HCP 关联依赖于 p58 的酪氨酸磷酸化。对应于 p58 尾部的磷酸酪氨酸肽在体外结合并激活 HCP。此外,将失活的突变体 HCP 引入 NK 细胞系可阻止 p58 介导的靶细胞裂解抑制。这些数据表明p58的抑制功能依赖于其酪氨酸磷酸化以及HCP的募集和激活。
更新日期:2019-11-01
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