Hashimoto S, Iwamatsu A, Ishiai M, Okawa K, Yamadori T, Matsushita M, Baba Y, Kishimoto T, Kurosaki T, Tsukada S
Department of Molecular Medicine, Osaka University Medical School, Osaka, Japan.
Blood. 1999 Oct 1;94(7):2357-64.
Bruton's tyrosine kinase (Btk) is a critical component in the B-cell antigen receptor (BCR)-coupled signaling pathway. Its deficiency in B cells leads to loss or marked reduction in the BCR-induced calcium signaling. It is known that this BCR-induced calcium signaling depends on the activation of phospholipase Cgamma (PLCgamma), which is mediated by Btk and another tyrosine kinase Syk and that the SH2 and pleckstrin homology (PH) domains of Btk play important roles in this activation process. Although the importance of the PH domain of Btk has been explained by its role in the membrane targeting of Btk, the functional significance of the SH2 domain in the calcium signaling has remained merely a matter of speculation. In this report, we identify that one of the major Btk-SH2 domain-binding proteins in B cells is BLNK (B-cell linker protein) and present evidences that the interaction of BLNK and the SH2 domain of Btk contributes to the complete tyrosine phosphorylation of PLCgamma.
布鲁顿酪氨酸激酶(Btk)是B细胞抗原受体(BCR)偶联信号通路中的关键成分。其在B细胞中的缺陷会导致BCR诱导的钙信号传导丧失或显著减少。已知这种BCR诱导的钙信号传导依赖于磷脂酶Cγ(PLCγ)的激活,而PLCγ的激活由Btk和另一种酪氨酸激酶Syk介导,并且Btk的SH2和普列克底物蛋白同源(PH)结构域在这一激活过程中发挥重要作用。尽管Btk的PH结构域的重要性已通过其在Btk膜靶向中的作用得到解释,但SH2结构域在钙信号传导中的功能意义仍只是一种推测。在本报告中,我们确定B细胞中主要的Btk-SH2结构域结合蛋白之一是BLNK(B细胞连接蛋白),并提供证据表明BLNK与Btk的SH2结构域的相互作用有助于PLCγ的完全酪氨酸磷酸化。