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