The G-CSF receptor carboxyl terminus, truncated in AML/SCN, is required for induction of a Stat5 protease activity.

Granulocyte colony-stimulating factor (G-CSF) has been shown to stimulate the activation of the signal transducer and activator of transcription 5 (Stat5). We show here that G-CSF-stimulated activation of Stat5 was attenuated when myeloid cells were induced to differentiate with G-CSF. Attenuated activation of Stat5 correlated with reduced Stat5 protein levels, which was associated with upregulation of a Stat5 protease activity. Carboxyl terminal truncation of the G-CSF receptor or expression of leukemogenic proteins Bcr-Abl and Tel-Jak2 abolished the upregulation of the Stat5 protease activity by G-CSF. These data add to our understanding of the roles of G-CSF and Stat5 in normal granulopoiesis and leukemogenesis.