Kurosaki T, Takata M, Yamanashi Y, Inazu T, Taniguchi T, Yamamoto T, Yamamura H
Department of Cardiovascular Molecular Biology, Lederle Laboratories, Pearl River, New York 10965.
J Exp Med. 1994 May 1;179(5):1725-9. doi: 10.1084/jem.179.5.1725.
Signaling through the B cell antigen receptor (BCR) results in rapid increases in tyrosine phosphorylation on a number of proteins. The BCR associates with two classes of tyrosine kinase: Src-family kinase (Src-protein-tyrosine kinase [PTK]; Lyn, Fyn, Blk, or Lck) and Syk kinase. We have investigated the interaction between the Src-PTK and the Syk kinase in the BCR signaling. In contrast to wild-type B cells, BCR-mediated tyrosine phosphorylation of Syk and activation of its in vitro kinase activity were profoundly reduced in lyn-negative cells. The requirement of the Src-PTK to induce tyrosine phosphorylation and activation of Syk was also demonstrated by cotransfection of syk and src-PTK cDNAs into COS cells. These results suggest that the Src-PTK associated with BCR phosphorylates the tyrosine residue(s) of Syk upon receptor stimulation, enhancing the activity of Syk.
通过B细胞抗原受体(BCR)发出的信号会导致多种蛋白质的酪氨酸磷酸化迅速增加。BCR与两类酪氨酸激酶相关联:Src家族激酶(Src蛋白酪氨酸激酶[PTK];Lyn、Fyn、Blk或Lck)和Syk激酶。我们研究了BCR信号传导中Src-PTK与Syk激酶之间的相互作用。与野生型B细胞相比,在lyn阴性细胞中,BCR介导的Syk酪氨酸磷酸化及其体外激酶活性的激活显著降低。将syk和src-PTK cDNA共转染到COS细胞中也证明了Src-PTK诱导Syk酪氨酸磷酸化和激活的必要性。这些结果表明,与BCR相关的Src-PTK在受体刺激时使Syk的酪氨酸残基磷酸化,增强了Syk的活性。