Syk in lymphocyte activation

B细胞抗原受体（BCR）的活化需要Syk蛋白酪氨酸激酶（PTK）的有效活化。缺陷的B细胞不能在受体接合后产生第二信使。此外，缺乏syk的小鼠不能发育正常数量的成熟B细胞。因此，Syk PTK在BCR的信号级联中起着必要的作用。虽然已经了解了很多关于Syk PTK，但仍然很少了解或了解该激酶如何调节B细胞活化。在本项目（项目1）中，我们将分析一种新的调节Syk活性的调节机制。此外，我们将使用真实的时间方法结合信号传导参数的分子解剖来分析Syk功能的动力学，所述信号传导参数在受体活化后调节B细胞形态中的细胞骨架改变。总之，这些研究可能会提供新的见解Syk如何调节B细胞活化，也了解Syk如何调节其他免疫细胞上的受体表达。

Activation of the B cell antigen receptor (BCR) requires the efficient activation of the Syk protein tyrosine kinase (PTK). B cells deficient are unable to generate second messengers following receptor engagement. Moreover, mice deficient in syk are unable to develop normal numbers of mature B cells. Hence, the Syk PTK plays a requisite role in the signaling cascade of the BCR. While much has been learned about the Syk PTK, there is still little appreciation or insight into how this kinase regulates B cell activation. In this project (Project 1), we will analyze a novel regulatory mechanism for regulating Syk activity. In addition, we will analyze the dynamics of Syk function using a real time approach combined with a molecular dissection of the signaling parameters which regulate cytoskeletal alterations in B cell morphology following receptor activation. Together, these studies will likely provide novel insights into how Syk regulates B cell activation and also insights into how Syk may regulate receptors expression on other immune cells.