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Analysis of Fes Kinase Activity in Myeloid Cell Growth and Differentiation

^a Departments of Biological Chemistry and Medicine, and the Molecular Biology Institute and Jonsson Comprehensive Cancer Center, UCLA School of Medicine, Los Angeles, California, USA;
^b Division of Research Immunology and Bone Marrow Transplantation, Children's Hospital of Los Angeles, Los Angeles, California, USA

Key Words. c-Fes. • Tyrosine kinase • Signal transduction • Cytokine • Myeloid cells

Dr. Judith C. Gasson, 11-934 Factor, Division of Hematology-Oncology, Department of Medicine, UCLA School of Medicine, Los Angeles, CA 90095-1678, USA.

Fes is a nonreceptor protein tyrosine kinase that has been implicated in a variety of cytokine signal transduction pathways, as well as differentiation of myeloid cells. To address the role of Fes in these processes, we overexpressed a kinase-defective Fes protein in the factor-dependent cell-lines, TF-1 and 32D. Proliferative responses to GM-CSF and interleukin 3, and the induction of differentiation by G-CSF were not altered by expression of the kinase mutant Fes protein, indicating that Fes kinase activity is not critical for these biological events in these cell lines.

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