原癌基因酪氨酸蛋白激酶Src
锡克
酪氨酸蛋白激酶
断点群集区域
受体酪氨酸激酶
Src家族激酶
SH2域
细胞生物学
布鲁顿酪氨酸激酶
激酶
B细胞受体
作者
Yuekang Xu,Kenneth W. Harder,Nicholas D. Huntington,Margaret L. Hibbs,David M. Tarlinton
出处
期刊:Immunity
[Elsevier]
日期:2005-01-01
卷期号:22 (1): 9-18
被引量:113
标识
DOI:10.1016/j.immuni.2004.12.004
摘要
Lyn, one of several Src-family tyrosine kinases in immune cells, is noted for its ability to negatively regulate signaling pathways through phosphorylation of inhibitory receptors, enzymes, and adaptors. Somewhat paradoxically, it is also a key mediator in several pathways of B cell activation, such as CD19 and CD180. Whether Lyn functions to promote or inhibit immune cell activation depends on the stimulus and the developmental state, meaning that the consequences of Lyn activity are context dependent. The importance of regulating Lyn activity is exemplified by the pathological conditions that develop in both lyn−/− and lyn gain-of-function mice (lynup/up), including lethal antibody-mediated autoimmune diseases and myeloid neoplasia. Here, we review the outcomes of altered Lyn activity within the framework of B cell development and differentiation and the circumstances that appear to dictate the outcome.
科研通智能强力驱动
Strongly Powered by AbleSci AI