Article
Oncogenic CALR mutant C-terminus mediates dual binding to the thrombopoietin receptor triggering complex dimerization and activation.
Nature communications - 5 Apr 2023
Papadopoulos Nicolas, Nédélec Audrey, Derenne Allison, Şulea Teodor Asvadur, Pecquet Christian, Chachoua Ilyas, Vertenoeil Gaëlle, Tilmant Thomas, Petrescu Andrei-Jose, Mazzucchelli Gabriel, Iorga Bogdan I, Vertommen Didier, Constantinescu Stefan N
Abstract excerpt
Calreticulin (CALR) frameshift mutations represent the second cause of myeloproliferative neoplasms (MPN). In healthy cells, CALR transiently and non-specifically interacts with immature N-glycosylated proteins through its N-terminal domain. Conversely, CALR frameshift mutants turn into rogue cytokines by stably and specifically interacting with the Thrombopoietin Receptor (TpoR), inducing its constitutive...
Topics
- Humans
- Dimerization
- Calreticulin
- Receptors, Thrombopoietin
- Frameshift Mutation
- Myeloproliferative Disorders
- Mutation
- Janus Kinase 2