T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form-Reference-Cited by-同舟云学术

T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form

Published:2020-02 Issue:1 Volume:523 Page:208-213
ISSN:0006-291X
Container-title:Biochemical and Biophysical Research Communications
language:en
Short-container-title:Biochemical and Biophysical Research Communications

Author:

Price Andrea,Druhan Lawrence J.^ORCID,Lance Amanda,Clark Gavin,Vestal C. Greer,Zhang Qing,Foureau David,Parsons Judy,Hamilton Alicia,Steuerwald Nury M.,Avalos Belinda R.

Funder

Leon Levine Foundation

Kerry and Simone Vickar Family Foundation

Publisher

Elsevier BV

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

Reference25 articles.

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2. Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML;Maxson;N. Engl. J. Med.,2013

3. Ligand independence of the T618I mutation in the colony-stimulating factor 3 receptor (CSF3R) protein results from loss of O-linked glycosylation and increased receptor dimerization;Maxson;J. Biol. Chem.,2014

4. Characterization of the leukemogenic potential of distal cytoplasmic CSF3R truncation and missense mutations;Zhang;Leukemia,2017

5. Gain-of-function mutations in granulocyte colony-stimulating factor receptor (CSF3R) reveal distinct mechanisms of CSF3R activation;Zhang;J. Biol. Chem.,2018

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