DELETION OF SRC HOMOLOGY-3 DOMAIN RESULTS IN CONSTITUTIVE ACTIVATION OF TEC PROTEIN-TYROSINE KINASE

Citation
Y. Yamashita et al., DELETION OF SRC HOMOLOGY-3 DOMAIN RESULTS IN CONSTITUTIVE ACTIVATION OF TEC PROTEIN-TYROSINE KINASE, Japanese journal of cancer research, 87(11), 1996, pp. 1106-1110
Citations number
26
Categorie Soggetti
Oncology
ISSN journal
09105050
Volume
87
Issue
11
Year of publication
1996
Pages
1106 - 1110
Database
ISI
SICI code
0910-5050(1996)87:11<1106:DOSHDR>2.0.ZU;2-H
Abstract
Tec protein-tyrosine kinase (PTK) is the prototype of a new subfamily of non-receptor type PTKs, and is abundantly expressed in hematopoieti c tissues. We have revealed that Tec is inducibly tyrosine-phosphoryla ted and activated by stimulation with a wide range of cytokines. To ge t more insight into the signaling mechanism through Tee, we have gener ated a constitutively active form of Tec PTK. Deletion of the Src homo logy (SH) 3 domain gave rise to a hyperphosphorylated and activated Te c kinase (Tec Delta SH3). The activity of Tec Delta SH3 was confirmed in 293 cells, as well as in cytokine-dependent hematopoietic cells (BA /F3). Tec Delta SH3 should be a useful tool to study the in vivo subst rates of Tec PTK.