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Paper Details

Unpaired Extracellular Cysteine Mutations of CSF3R Mediate Gain or Loss of Function.
Cancer Res
8
2017
CSF3R, CSF3R cytoplasmic truncation, CSF3R extracellular domain, Cysteine, G-CSF receptor, JAK, W341C, W791X, allele, cells, chronic neutrophilic leukemia, congenital and idiopathic neutropenia, cysteine, cysteines, disulfide, fibronectin-like type III domain, leukemia, leukocytosis, patient, patients, transformed, transformed cells
Aged, Animals, Cysteine, Exome, Female, HEK293 Cells, Humans, Leukemia, Myeloid, Acute, Mice, Mutation, Missense, NIH 3T3 Cells, Phenotype, Receptors, Colony-Stimulating Factor
Author NameAffiliation
Haijiao ZhangOregon Health & Science University Knight Cancer Institute
Sophie MeansOregon Health & Science University Knight Cancer Institute
Anna Reister SchultzOregon Health & Science University Knight Cancer Institute
Kevin Watanabe-SmithOregon Health & Science University Knight Cancer Institute
Bruno C MedeirosStanford University School of Medicine
Daniel BottomlyDepartment of Medical Informatics and Clinical Epidemiology, Oregon Health & Science University Knight Cancer Institute
Beth WilmotDepartment of Medical Informatics and Clinical Epidemiology, Oregon Health & Science University Knight Cancer Institute
Shannon K McWeeneyDepartment of Medical Informatics and Clinical Epidemiology, Oregon Health & Science University Knight Cancer Institute
Tim K??kensh??nerSwiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Federale de Lausanne (EPFL)
Oliver HantschelSwiss Institute for Experimental Cancer Research (ISREC), Ecole Polytechnique Federale de Lausanne (EPFL)
Jeffrey W TynerOregon Health & Science University Knight Cancer Institute
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