Article
T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form.
Biochemical and biophysical research communications - 26 Feb 2020
Price Andrea, Druhan Lawrence J, Lance Amanda, Clark Gavin, Vestal C Greer, Zhang Qing, Foureau David, Parsons Judy, Hamilton Alicia, Steuerwald Nury M, Avalos Belinda R
Abstract excerpt
Activating mutations in the membrane-proximal region of the colony-stimulating factor 3 receptor (CSF3R) are a hallmark of chronic neutrophilic leukemia (CNL) with the T618I mutation being most common. The mechanisms underlying constitutive activation of the T618I CSF3R and its signal propagation are poorly understood. Ligand-independent activation of the T618I CSF3R has previously been attributed to loss of...
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