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Deletion of Src Homology 3 Domain Results in Constitutive Activation of Tec Protein‐Tyrosine Kinase

机译:Src同源性3域的删除导致Tec蛋白酪氨酸激酶的组成性激活

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摘要

Tec protein‐tyrosine kinase (PTK) is the prototype of a new subfamily of non‐receptor type PTKs, and is abundantly expressed in hematopoietic tissues. We have revealed that Tec is inducibly tyrosine‐phosphorylated and activated by stimulation with a wide range of cytokines. To get more insight into the signaling mechanism through Tec, we have generated a constitutively active form of Tec PTK. Deletion of the Src homology (SH) 3 domain gave rise to a hyperphosphorylated and activated Tec kinase (TecΔSH3). The activity of TecΔSH3 was confirmed in 293 cells, as well as in cytokine‐dependent hematopoietic cells (BA/F3). TecΔSH3 should be a useful tool to study the in vivo substrates of Tec PTK.
机译:Tec蛋白酪氨酸激酶(PTK)是非受体型PTK的一个新亚家族的原型,在造血组织中大量表达。我们发现,Tec可诱导酪氨酸磷酸化并通过多种细胞因子刺激而被激活。为了通过Tec深入了解信号传导机制,我们生成了Tec PTK的组成型活性形式。 Src同源性(SH)3结构域的删除产生了高磷酸化和活化的Tec激酶(TecΔSH3)。在293细胞以及依赖细胞因子的造血细胞(BA / F3)中证实了TecΔSH3的活性。 TecΔSH3应该是研究Tec PTK体内底物的有用工具。

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