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Article

Thrombopoietin is required for full phenotype expression in a JAK2V617F transgenic mouse model of polycythemia vera.

PloS one - 1 Jan 2020

Spivak Jerry L, Merchant Akil, Williams Donna M, Rogers Ophelia, Zhao Wanke, Duffield Amy, Resar Linda S, Moliterno Alison R, Zhao Zhizhuang J

Abstract excerpt

The myeloproliferative neoplasms, polycythemia vera, essential thrombocytosis and primary myelofibrosis are hematopoietic stem cell disorders and share driver mutations that either directly activate the thrombopoietin receptor, MPL, or activate it indirectly through gain-of-function mutations in the gene for JAK2, its cognate tyrosine kinase. Paradoxically, MPL surface expression in hematopoietic stem cells is...

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Identifiers

PMID: 32479500
DOI: 10.1371/journal.pone.0232801
PMCID: PMC7263591

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Thrombopoietin is required for full phenotype expression in a JAK2V617F transgenic mouse model of polycythemia vera.PMID 32479500Read ↗

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