The thrombopoietin receptor, MPL, is critical for development of a JAK2V617F-induced myeloproliferative neoplasm
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Title
The thrombopoietin receptor, MPL, is critical for development of a JAK2V617F-induced myeloproliferative neoplasm
Authors
Keywords
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Journal
BLOOD
Volume 124, Issue 26, Pages 3956-3963
Publisher
American Society of Hematology
Online
2014-10-23
DOI
10.1182/blood-2014-07-587238
References
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Note: Only part of the references are listed.- A novel activating, germline JAK2 mutation, JAK2R564Q, causes familial essential thrombocytosis
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- Mpl expression on megakaryocytes and platelets is dispensable for thrombopoiesis but essential to prevent myeloproliferation
- (2014) A. P. Ng et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Somatic CALR Mutations in Myeloproliferative Neoplasms with Nonmutated JAK2
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- Somatic Mutations of Calreticulin in Myeloproliferative Neoplasms
- (2013) Thorsten Klampfl et al. NEW ENGLAND JOURNAL OF MEDICINE
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- New mutations and pathogenesis of myeloproliferative neoplasms
- (2011) W. Vainchenker et al. BLOOD
- Mouse models of myeloproliferative neoplasms: JAK of all grades
- (2011) J. Li et al. Disease Models & Mechanisms
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- (2011) Fu-Sheng Chou et al. JOURNAL OF CELLULAR BIOCHEMISTRY
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- (2011) Ayalew Tefferi et al. NEW ENGLAND JOURNAL OF MEDICINE
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- (2010) C. Marty et al. BLOOD
- Conditional expression of heterozygous or homozygous Jak2V617F from its endogenous promoter induces a polycythemia vera-like disease
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- Safety and Efficacy of INCB018424, a JAK1 and JAK2 Inhibitor, in Myelofibrosis
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- (2009) K. Liu et al. HAEMATOLOGICA
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- (2008) A Tefferi et al. LEUKEMIA
- Ratio of mutant JAK2-V617F to wild-type Jak2 determines the MPD phenotypes in transgenic mice
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