Abstract
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 language | English (US) |
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Pages (from-to) | 2630-2631 |
Number of pages | 2 |
Journal | Blood |
Volume | 133 |
Issue number | 25 |
DOIs | |
State | Published - 2019 |
ASJC Scopus subject areas
- Biochemistry
- Immunology
- Hematology
- Cell Biology