title: Molecular Mechanism of Mutant CALR-Mediated Transformation.
abstract: Elf and colleagues used an elegant series of functional and biochemical assays to investigate the molecular mechanism of mutant calreticulin (CALR)-driven cellular transformation in myeloproliferative neoplasms (MPN). Mutant CALR is sufficient to induce MPN in mouse transplantation experiments, and transformation is dependent upon physical interaction mediated by the positive electrostatic charge of the mutant CALR C-terminal domain and the thrombopoietin receptor MPL.
authors.affiliation: Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York.
authors.forename: Robert F
authors.initials: RF
authors.lastname: Stanley
authors.affiliation: Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York. Department of Medicine, Albert Einstein College of Medicine-Montefiore Medical Center, Bronx, New York. Albert Einstein Cancer Center, Albert Einstein College of Medicine, Bronx, New York. Ruth L. and David S. Gottesman Institute for Stem Cell Biology and Regenerative Medicine, Albert Einstein College of Medicine, Bronx, New York. ulrich.steidl@einstein.yu.edu.
authors.forename: Ulrich
authors.initials: U
authors.lastname: Steidl
mesh_terms: D000818:Animals; D002471:Cell Transformation, Neoplastic; D053614:Janus Kinase 2; D009154:Mutation; D009196:Myeloproliferative Disorders
chemical_list: D053614:Janus Kinase 2