| Literature DB >> 27045016 |
Robert F Stanley1, Ulrich Steidl2.
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. ©2016 American Association for Cancer Research.Entities:
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Year: 2016 PMID: 27045016 PMCID: PMC4832981 DOI: 10.1158/2159-8290.CD-16-0238
Source DB: PubMed Journal: Cancer Discov ISSN: 2159-8274 Impact factor: 39.397