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不同的p53/56lyn和p59fyn结构域与未磷酸化和磷酸化的Ig-α相关联。

Distinct p53/56lyn and p59fyn domains associate with nonphosphorylated and phosphorylated Ig-alpha.

作者信息

Pleiman C M, Abrams C, Gauen L T, Bedzyk W, Jongstra J, Shaw A S, Cambier J C

机构信息

Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206.

出版信息

Proc Natl Acad Sci U S A. 1994 May 10;91(10):4268-72. doi: 10.1073/pnas.91.10.4268.

Abstract

Among the earliest detectable events in B-cell antigen receptor-mediated signal transduction are the activation of receptor-associated Src-family tyrosine kinases and the tyrosine phosphorylation of Ig-alpha and Ig-beta receptor subunits. These kinases appear to interact with resting B-cell antigen receptor complexes primarily through the Ig-alpha chain antigen receptor homology 1 (ARH1) motif. Recent studies showed a dramatic increase in the amount of Src-family kinase p59fyn bound to Ig-alpha when ARH1 motif tyrosines were phosphorylated. To explore the submolecular basis of these interactions, we conducted mutational analysis to localize sites in p53/56lyn and p59fyn that bind nonphosphorylated and phosphorylated Ig-alpha. Here we report that distinct regions within these kinases bind nonphosphorylated and phosphorylated Ig-alpha ARH1 motifs. The N-terminal 10 residues mediate binding to the nonphosphorylated Ig-alpha ARH1 motif. Association with the phosphorylated Ig-alpha ARH1 motif is mediated by Src homology 2 domains. These findings suggest a mechanism whereby ligand-induced Ig-alpha tyrosine phosphorylation initiates a change in the orientation of an associated kinase that may alter its activity and/or access to substrates and other effectors.

摘要

在B细胞抗原受体介导的信号转导中,最早可检测到的事件之一是受体相关Src家族酪氨酸激酶的激活以及Ig-α和Ig-β受体亚基的酪氨酸磷酸化。这些激酶似乎主要通过Ig-α链抗原受体同源性1(ARH1)基序与静止的B细胞抗原受体复合物相互作用。最近的研究表明,当ARH1基序酪氨酸磷酸化时,与Ig-α结合的Src家族激酶p59fyn的量会急剧增加。为了探究这些相互作用的亚分子基础,我们进行了突变分析,以定位p53/56lyn和p59fyn中与未磷酸化和磷酸化Ig-α结合的位点。在此我们报告,这些激酶内的不同区域与未磷酸化和磷酸化的Ig-α ARH1基序结合。N端的10个残基介导与未磷酸化的Ig-α ARH1基序的结合。与磷酸化的Ig-α ARH1基序的结合由Src同源2结构域介导。这些发现提示了一种机制,即配体诱导的Ig-α酪氨酸磷酸化引发相关激酶方向的改变,这可能会改变其活性和/或对底物及其他效应器的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a3d9/43766/42674dec9f2f/pnas01132-0176-a.jpg

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