Mutated CALR: Tails from the crypt

Research output: Contribution to journalReview articlepeer-review

2 Scopus citations


The discovery by exome sequencing that calreticulin (CALR) gene mutations are important gain-of-function myeloproliferative neoplasm (MPN) driver mutations1,2 was as inexplicable as it was unexpected. In this issue of Blood, Pecquet et al3 report that mutated CALR behaves like a rogue chaperone, usurping the role of JAK2 and promiscuously transporting immature or trafficdefective thrombopoietin receptors (TpoRs) to the cell surface from the endoplasmic reticulum (ER) (see figure).

Original languageEnglish (US)
Pages (from-to)2630-2631
Number of pages2
Issue number25
StatePublished - 2019

ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology


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