O'Shea J J, Ashwell J D, Bailey T L, Cross S L, Samelson L E, Klausner R D
Biological Response Modifiers Program, PRI/DynCorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701-1201.
Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1741-5. doi: 10.1073/pnas.88.5.1741.
Ligand binding to the T-cell antigen receptor results in phosphatidylinositol hydrolysis and the resultant activation of protein kinase C, as well as the activation of a receptor-coupled protein-tyrosine kinase. As a model for tyrosine kinase activation in T cells, we used retroviral gene transfer to express the v-src oncogene in an antigen-specific murine T-cell hybridoma. Clones that expressed v-src mRNA demonstrated constitutive tyrosine phosphorylation of several cellular substrates, including the zeta chain of the T-cell receptor, and constitutive interleukin 2 production. Thus, expression of a constitutively active protein-tyrosine kinase such as pp60v-src appears to be sufficient to induce the expression of at least one gene critical to the process of T-cell activation.