Molecular mechanism of mutant CALR–Mediated transformation

Robert F. Stanley, Ulrich G. Steidl

Research output: Contribution to journalArticle

4 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)344-346
Number of pages3
JournalCancer Discovery
Volume6
Issue number4
DOIs
StatePublished - Apr 1 2016

ASJC Scopus subject areas

  • Oncology

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