Deletion of Src homology 3 domain results in constitutive activation of Tec protein-tyrosine kinase.

Abstract

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.