ArticleBlood2010
JAK2 V617F impairs hematopoietic stem cell function in a conditional knock-in mouse model of JAK2 V617F-positive essential thrombocythemia.
Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
124 citing papers in PubMed, 203 citations in OpenAlex.
- Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.Biomarker research · 2026Review
- Article
- Targeting mitochondrial dysfunction in myeloproliferative neoplasms: current strategies and future directions - a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Clonal hematopoiesis and hematological malignancy.The Journal of clinical investigation · 2024Review
- Exploiting Synthetic Lethality between Germline BRCA1 Haploinsufficiency and PARP Inhibition in JAK2V617F-Positive Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Article
- Complementary and countervailing actions of Jak2 and Ikk2 in hematopoiesis in mice.Experimental hematology · 2023Article
- Splanchnic Vein Thrombosis in Myelofibrosis-An Underappreciated Hallmark of Disease Phenotype.International journal of molecular sciences · 2023Review
- Different niches for stem cells carrying the same oncogenic driver affect pathogenesis and therapy response in myeloproliferative neoplasms.Nature cancer · 2023Article
- The novel GATA1-interacting protein HES6 is an essential transcriptional cofactor for human erythropoiesis.Nucleic acids research · 2023Article
- Inhibition of ERK1/2 signaling prevents bone marrow fibrosis by reducing osteopontin plasma levels in a myelofibrosis mouse model.Leukemia · 2023Article
- Clonal hematopoiesis and bone marrow inflammation.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Targeting pleckstrin-2/Akt signaling reduces proliferation in myeloproliferative neoplasm models.The Journal of clinical investigation · 2023Article
- Mechanisms of platelet activation in cancer-associated thrombosis: a focus on myeloproliferative neoplasms.Frontiers in cell and developmental biology · 2023Review
- Identification of curaxin as a potential new therapeutic for JAK2 V617F mutant patients.PloS one · 2023Article
- The ERK2-DBP domain opposes pathogenesis of a mouse JAK2V617F-driven myeloproliferative neoplasm.Blood · 2022Article
- JAK2V617F Mutant Megakaryocytes Contribute to Hematopoietic Aging in a Murine Model of Myeloproliferative Neoplasm.Stem cells (Dayton, Ohio) · 2022Article
- Characterization of disease-propagating stem cells responsible for myeloproliferative neoplasm-blast phase.JCI insight · 2022Article
- Article
- Insights into the Potential Mechanisms of JAK2V617F Somatic Mutation Contributing Distinct Phenotypes in Myeloproliferative Neoplasms.International journal of molecular sciences · 2022Review
64 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
The JAK2 V617F mutation is found in most patients with a myeloproliferative neoplasm and is sufficient to produce a myeloproliferative phenotype in murine retroviral transplantation or transgenic models. However, several lines of evidence suggest that disease phenotype is influenced by the level of mutant JAK2 signaling, and we have therefore generated a conditional knock-in mouse in which a human JAK2 V617F is expressed under the control of the mouse Jak2 locus. Human and murine Jak2 transcripts are expressed at similar levels, and mice develop modest increases in hemoglobin and platelet levels reminiscent of human JAK2 V617F-positive essential thrombocythemia. The phenotype is transplantable and accompanied by increased terminal erythroid and megakaryocyte differentiation together with increased numbers of clonogenic progenitors, including erythropoietin-independent erythroid colonies. Unexpectedly, JAK2(V617F) mice develop reduced numbers of lineage(-)Sca-1(+)c-Kit(+) cells, which exhibit increased DNA damage, reduced apoptosis, and reduced cell cycling. Moreover, competitive bone marrow transplantation studies demonstrated impaired hematopoietic stem cell function in JAK2(V617F) mice. These results suggest that the chronicity of human myeloproliferative neoplasms may reflect a balance between impaired hematopoietic stem cell function and the accumulation of additional mutations.
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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.