Activation of the thrombopoietin receptor by mutant calreticulin in CALR-mutant myeloproliferative neoplasms

Recurrent somatic mutations of calreticulin (CALR) have been identified in patients harboring myeloproliferative neoplasms; however, their role in tumorigenesis remains elusive. Here, we found that the expression of mutant but not wild-type CALR induces the thrombopoietin (TPO)-independent growth of...

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Veröffentlicht in:	Blood 2016-03, Vol.127 (10), p.1307-1316
Hauptverfasser:	Araki, Marito, Yang, Yinjie, Masubuchi, Nami, Hironaka, Yumi, Takei, Hiraku, Morishita, Soji, Mizukami, Yoshihisa, Kan, Shin, Shirane, Shuichi, Edahiro, Yoko, Sunami, Yoshitaka, Ohsaka, Akimichi, Komatsu, Norio
Format:	Artikel
Sprache:	eng
Schlagworte:	Calreticulin - genetics Calreticulin - metabolism Cell Line, Tumor HEK293 Cells Hematologic Neoplasms - genetics Hematologic Neoplasms - metabolism Hematologic Neoplasms - mortality Humans Induced Pluripotent Stem Cells - metabolism Induced Pluripotent Stem Cells - pathology Janus Kinase 2 - metabolism Myeloproliferative Disorders - genetics Myeloproliferative Disorders - metabolism Myeloproliferative Disorders - pathology Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Phosphorylation Protein Structure, Tertiary Receptors, Thrombopoietin - genetics Receptors, Thrombopoietin - metabolism Thrombopoiesis - genetics Thrombopoietin - metabolism
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