Pandey A, Fernandez M M, Steen H, Blagoev B, Nielsen M M, Roche S, Mann M, Lodish H F
Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA.
J Biol Chem. 2000 Dec 8;275(49):38633-9. doi: 10.1074/jbc.M007849200.
In an effort to clone novel tyrosine-phosphorylated substrates of the epidermal growth factor receptor, we have initiated an approach coupling affinity purification using anti-phosphotyrosine antibodies to mass spectrometry-based identification. Here, we report the identification of a signaling molecule containing a Src homology 3 domain as well as an immunoreceptor tyrosine-based activation motif (ITAM). This molecule is 55% identical to a previously isolated molecule designated signal transducing adaptor molecule (STAM) that was identified as an interleukin (IL)-2-induced phosphoprotein and is therefore designated STAM2. Tyrosine phosphorylation of STAM2 is induced by growth factors such as epidermal growth factor and platelet-derived growth factor as well as by cytokines like IL-3. Several of the deletion mutants tested except the one containing only the amino-terminal region underwent tyrosine phosphorylation upon growth factor stimulation, implying that STAM2 is phosphorylated on several tyrosine residues. STAM2 is downstream of the Jak family of kinases since coexpression of STAM2 with Jak1 or Jak2 but not an unrelated Tec family kinase, Etk, resulted in its tyrosine phosphorylation. In contrast to epidermal growth factor receptor-induced phosphorylation, this required the ITAM domain since mutants lacking this region did not undergo tyrosine phosphorylation. Finally, overexpression of wild type STAM2 led to an increase in IL-2-mediated induction of c-Myc promoter activation indicating that it potentiates cytokine receptor signaling.
为了克隆表皮生长因子受体新的酪氨酸磷酸化底物,我们启动了一种方法,即将使用抗磷酸酪氨酸抗体的亲和纯化与基于质谱的鉴定相结合。在此,我们报告鉴定出一种含有Src同源3结构域以及基于免疫受体酪氨酸的激活基序(ITAM)的信号分子。该分子与先前分离的名为信号转导衔接分子(STAM)的分子有55%的同源性,STAM被鉴定为白细胞介素(IL)-2诱导的磷蛋白,因此将其命名为STAM2。表皮生长因子和血小板衍生生长因子等生长因子以及IL-3等细胞因子可诱导STAM2的酪氨酸磷酸化。除了仅含氨基末端区域的缺失突变体之外,所测试的几个缺失突变体在生长因子刺激后都发生了酪氨酸磷酸化,这意味着STAM2在多个酪氨酸残基上被磷酸化。STAM2位于Jak激酶家族的下游,因为STAM2与Jak1或Jak2共表达可导致其酪氨酸磷酸化,而与不相关的Tec家族激酶Etk共表达则不会。与表皮生长因子受体诱导的磷酸化不同,这需要ITAM结构域,因为缺乏该区域的突变体不会发生酪氨酸磷酸化。最后,野生型STAM2的过表达导致IL-2介导的c-Myc启动子激活增加,表明它增强了细胞因子受体信号传导。