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

Jpn J Cancer Res. 1996 Nov;87(11):1106-10. doi: 10.1111/j.1349-7006.1996.tb03118.x.

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 (Tec deltaSH3). The activity of Tec deltaSH3 was confirmed in 293 cells, as well as in cytokine-dependent hematopoietic cells (BA/F3). Tec deltaSH3 should be a useful tool to study the in vivo substrates of Tec PTK.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Binding Sites
  • Enzyme Activation
  • Gene Deletion*
  • Mice
  • Phosphorylation
  • Protein-Tyrosine Kinases / metabolism*
  • Signal Transduction / physiology
  • src Homology Domains*

Substances

  • Tec protein-tyrosine kinase
  • Protein-Tyrosine Kinases