Mutant calreticulin interacts with MPL in the secretion pathway for activation on the cell surface

Studies have shown that mutant calreticulin (CALR) constitutively activates the thrombopoietin (TPO) receptor MPL and thus plays a causal role in the development of myeloproliferative neoplasms (MPNs). To further elucidate the molecular mechanism by which mutant CALR promotes MPN development, we stu...

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Veröffentlicht in:	Leukemia 2020-02, Vol.34 (2), p.499-509
Hauptverfasser:	Masubuchi, Nami, Araki, Marito, Yang, Yinjie, Hayashi, Erina, Imai, Misa, Edahiro, Yoko, Hironaka, Yumi, Mizukami, Yoshihisa, Kihara, Yoshihiko, Takei, Hiraku, Nudejima, Mai, Koike, Masato, Ohsaka, Akimichi, Komatsu, Norio
Format:	Artikel
Sprache:	eng
Schlagworte:	13/1 13/31 13/95 14/19 631/67/1990/2331 631/80/86 82/80 Antibodies Calcium-binding proteins Calreticulin Calreticulin - genetics Cancer Research Cell activation Cell culture Cell Line Cell surface Cell Transformation, Neoplastic - genetics Critical Care Medicine Development and progression Gene mutations Genetic aspects Glycan Golgi apparatus Health aspects Hematology Humans Intensive Internal Medicine Localization Medicine Medicine & Public Health Mutants Mutation Mutation - genetics Myelofibrosis Myeloproliferative Disorders - genetics Neoplasms Oncogenes Oncology Plasmids Protein transport Receptors, Thrombopoietin - genetics Secretion Secretory Pathway - genetics Shutdowns Signal Transduction - genetics Thrombocythemia Thrombocytosis Thrombopoietin Trypsin Trypsin - genetics Tumors University graduates
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