Regulation of Ack-Family Nonreceptor Tyrosine Kinases
Author(s) -
Victoria Prieto-Echagüe,
W. Todd Miller
Publication year - 2011
Publication title -
journal of signal transduction
Language(s) - English
Resource type - Journals
eISSN - 2090-1739
pISSN - 2090-1747
DOI - 10.1155/2011/742372
Subject(s) - autophosphorylation , microbiology and biotechnology , tyrosine kinase , receptor tyrosine kinase , phosphorylation , kinase , tyrosine phosphorylation , protein kinase domain , signal transduction , cancer research , medicine , biology , protein kinase a , biochemistry , mutant , gene
Ack family non-receptor tyrosine kinases are unique with regard to their domain composition and regulatory properties. Human Ack1 (activated Cdc42-associated kinase) is ubiquitously expressed and is activated by signals that include growth factors and integrin-mediated cell adhesion. Stimulation leads to Ack1 autophosphorylation and to phosphorylation of additional residues in the C-terminus. The N-terminal SAM domain is required for full activation. Ack1 exerts some of its effects via protein-protein interactions that are independent of its kinase activity. In the basal state, Ack1 activity is suppressed by an intramolecular interaction between the catalytic domain and the C-terminal region. Inappropriate Ack1 activation and signaling has been implicated in the development, progression, and metastasis of several forms of cancer. Thus, there is increasing interest in Ack1 as a drug target, and studies of the regulatory properties of the enzyme may reveal features that can be exploited in inhibitor design.
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