ArticleBlood2008
Transgenic expression of JAK2V617F causes myeloproliferative disorders in mice.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed, 211 citations in OpenAlex.
- Hypoxia-inducible factors contribute to venous thrombosis in a mouse model of myeloproliferative neoplasms.Blood advances · 2026Article
- Sabotaged Integral HSC Heterogeneity Underlies Essential Thrombocythemia Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Leukemia-expanded splenic CD81+ erythroblasts potentiate disease progression in mice by reshaping leukemic cell metabolism.The Journal of clinical investigation · 2025Article
- Efficacy of JAK1/2 inhibition in murine myeloproliferative neoplasms is not mediated by targeting oncogenic signaling.Nature communications · 2025Article
- Pathogenesis and management of high molecular risk myeloproliferative neoplasms.Haematologica · 2025Review
- Overexpression of miR-99a promoted expansion and suppressed differentiation of hematopoietic stem/progenitor cells.Scientific reports · 2025Article
- Myeloproliferative Neoplasms: Challenging Dogma.Journal of clinical medicine · 2024Review
- Engineering a humanized animal model of polycythemia vera with minimalHaematologica · 2024Article
- Newly identified roles for PIEZO1 mechanosensor in controlling normal megakaryocyte development and in primary myelofibrosis.American journal of hematology · 2024Article
- Article
- Mechanisms of platelet activation in cancer-associated thrombosis: a focus on myeloproliferative neoplasms.Frontiers in cell and developmental biology · 2023Review
- Article
- JAK2V617F Mutant Megakaryocytes Contribute to Hematopoietic Aging in a Murine Model of Myeloproliferative Neoplasm.Stem cells (Dayton, Ohio) · 2022Article
- Inhibition of Osteoblast Differentiation by JAK2Frontiers in oncology · 2022Article
- A Murine Model With JAK2V617F Expression in Both Hematopoietic Cells and Vascular Endothelial Cells Recapitulates the Key Features of Human Myeloproliferative Neoplasm.Frontiers in oncology · 2021Article
- The Thrombopoietin Receptor, MPL, Is a Therapeutic Target of Opportunity in the MPN.Frontiers in oncology · 2021Review
- Lysyl oxidase inhibition in primary myelofibrosis: A renewed strategy.Archives of stem cell and therapy · 2020Article
- The role of clonal haematopoiesis in cardiovascular diseases: epidemiology and experimental studies.Journal of internal medicine · 2020Review
- Platelet Dysfunction and Thrombosis in JAK2Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Murine Models of Myelofibrosis.Cancers · 2020Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The JAK2(V617F) mutation was found in most patients with myeloproliferative disorders (MPDs), including polycythemia vera, essential thrombocythemia, and primary myelofibrosis. We have generated transgenic mice expressing the mutated enzyme in the hematopoietic system driven by a vav gene promoter. The mice are viable and fertile. One line of the transgenic mice, which expressed a lower level of JAK2(V617F), showed moderate elevations of blood cell counts, whereas another line with a higher level of JAK2(V617F) expression displayed marked increases in blood counts and developed phenotypes that closely resembled human essential thrombocythemia and polycythemia vera. The latter line of mice also developed primary myelofibrosis-like symptoms as they aged. The transgenic mice showed erythroid, megakaryocytic, and granulocytic hyperplasia in the bone marrow and spleen, displayed splenomegaly, and had reduced levels of plasma erythropoietin and thrombopoietin. They possessed an increased number of hematopoietic progenitor cells in peripheral blood, spleen, and bone marrow, and these cells formed autonomous colonies in the absence of growth factors and cytokines. The data show that JAK2(V617F) can cause MPDs in mice. Our study thus provides a mouse model to study the pathologic role of JAK2(V617F) and to develop treatment for MPDs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.