ArticleExperimental hematology & oncology2015
Identification of AIM2 as a downstream target of JAK2V617F.
Article in Experimental hematology & oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- NLRP3-induced systemic inflammation controls the development of JAK2V617F mutant myeloproliferative neoplasms.Nature communications · 2025Article
- Article
- Chronic Inflammation in Primary Myelofibrosis: In-Depth Insights Into Pathogenesis and Promising Anti-Inflammatory Therapeutic Strategies.Mediators of inflammation · 2025Review
- Nucleic acid-induced inflammation on hematopoietic stem cells.Experimental hematology · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Putative Role of Neutrophil Extracellular Trap Formation in Chronic Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Biological drivers of clinical phenotype in myelofibrosis.Leukemia · 2023Review
- High cell-free DNA is associated with disease progression, inflammasome activation and elevated levels of inflammasome-related cytokine IL-18 in patients with myelofibrosis.Frontiers in immunology · 2023Article
- The inflammasomes: crosstalk between innate immunity and hematology.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Systemic Optimization of Gene Electrotransfer Protocol Using Hard-to-Transfect UT-7 Cell Line as a Model.Biomedicines · 2022Article
- Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation.International journal of molecular sciences · 2022Review
- Inflammasomes and the Maintenance of Hematopoietic Homeostasis: New Perspectives and Opportunities.Molecules (Basel, Switzerland) · 2021Review
- Genetics and Pathogenetic Role of Inflammasomes in Philadelphia Negative Chronic Myeloproliferative Neoplasms: A Narrative Review.International journal of molecular sciences · 2021Review
- Inflammasome Activation in Myeloid Malignancies-Friend or Foe?Frontiers in cell and developmental biology · 2021Review
- Inflammasome as an Effective Platform for Fibrosis Therapy.Journal of inflammation research · 2021Review
- Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR-ABL-Negative Myeloproliferative Neoplasm.Antioxidants (Basel, Switzerland) · 2020Review
- The Role of Inflammation and Inflammasome in Myeloproliferative Disease.Journal of clinical medicine · 2020Review
- Article
- Significance of combined detection of JAK2V617F, MPL and CALR gene mutations in patients with essential thrombocythemia.Experimental and therapeutic medicine · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe gain-of-function mutation JAK2V617F is frequently found in Philadelphia-chromosome-negative myeloproliferative neoplasm (MPN) patients. However, the tumorigenic properties of JAK2V617F have mostly been characterized in in vivo and in vitro murine models due to the lack of appropriate human cell lines.
methodsUsing the multipotent hematologic cell line UT-7/GM, we established D9, a novel human cell line that expresses JAK2V617F upon tetracycline addition. We assessed cellular differentiation in UT-7/GM cells when JAK2V617F was induced, and we used microarrays to analyze changes in mRNA expression caused by JAK2V617F.
resultsUsing the human D9 cell line, we demonstrated that the induction of JAK2V617F leads to cytokine-independent cell growth with increased STAT activation and erythroid differentiation, mimicking the characteristics observed in polycythemia vera, making it a suitable in vitro model for studying this disorder. Interestingly, JAK2V617F-dependent erythroid cell differentiation was blocked when GM-CSF was added to the culture, suggesting that the GM-CSF pathway antagonizes JAK2V617F-induced erythroid cell differentiation. Our microarray analysis identified several genes involved in inflammasome activation, such as AIM2, IL1B, and CASP1, which were significantly up-regulated in JAK2V617F-induced cells.
conclusionsThe observed inflammasome activation following JAK2V617F induction is consistent with a recent report demonstrating the involvement of IL1B in myelofibrosis development in a JAK2V617F model mouse. These results indicate that the D9 cell line should be useful for characterizing the signaling pathways downstream of JAK2V617F, allowing for the identification of effector molecules that contribute to the development of MPN.
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