Granulocyte colony‐stimulating factor induces the binding of STAT1 and STAT3 to the IFNγ response region within the promoter of the FcγRI/CD64 gene in human neutrophils

FEBS Letters

Cassatella, Marco A.¹  Bovolenta, Chiara¹  Gasperini, Sara¹ 

[1]Department of General Pathology and Department of Biochemistry, University of Verona, Strada le Grazie 8, 37134 Verona, Italy

关键词: Neutrophil;    G-CSF;    FcγRI/CD64;    STAT1;    STAT3;   

DOI  :  10.1016/0014-5793(96)00453-X

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Granulocyte colony-stimulating factor (G-CSF) has been recently shown to induce the high-affinity Fc receptor for IgG (FcγRI/CD64) in human polymorphonuclear neutrophils (PMN). To elucidate the molecular mechanisms whereby G-CSF exerts this effect, we examined whether the cytokine induces the binding of transcription factors to the IFNγ response region (GRR), a well characterized regulatory element in the FCγRI promoter that is responsible for the transcriptional induction of this gene. Using electrophoretic mobility shift assays, we show that in human PMN, G-CSF activates a GRR-binding complex which contains members of the signal transducer and activator of transcription (STAT) family of proteins, namely STAT1 and STAT3. In keeping with this result, treatment of neutrophils with G-CSF led to tyrosine phosphorylation of STAT3, as determined by immunoprecipitation followed by immunoblotting with antiphosphotyrosine antibodies. This is the first demonstration that in human neutrophils, the induction by G-CSF of FcγRI gene expression may be mediated by the binding of STAT1 and STAT3 to the GRR sequence.

【 授权许可】

Unknown