ArticleBlood2012
Critical requirement for Stat5 in a mouse model of polycythemia vera.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
72 citing papers in PubMed, 132 citations in OpenAlex.
- Taurine attenuates polystyrene microplastic-associated oxidative stress, inflammation, and apoptotic changes in the spleen of mice.Frontiers in pharmacology · 2026Article
- Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms.Cancer discovery · 2024Article
- Activating mutations in JAK2 and CALR differentially affect intracellular calcium flux in store operated calcium entry.Cell communication and signaling : CCS · 2024Article
- Review
- Targeting of STAT5 using the small molecule topotecan hydrochloride suppresses acute myeloid leukemia progression.Oncology reports · 2023Article
- SRSF2-P95H decreases JAK/STAT signaling in hematopoietic cells and delays myelofibrosis development in mice.Leukemia · 2023Article
- A selective small-molecule STAT5 PROTAC degrader capable of achieving tumor regression in vivo.Nature chemical biology · 2023Article
- Putative Role of Neutrophil Extracellular Trap Formation in Chronic Myeloproliferative Neoplasms.International journal of molecular sciences · 2023Review
- Neutrophil Death in Myeloproliferative Neoplasms: Shedding More Light on Neutrophils as a Pathogenic Link to Chronic Inflammation.International journal of molecular sciences · 2022Review
- Article
- Philadelphia-Negative MPN: A Molecular Journey, from Hematopoietic Stem Cell to Clinical Features.Medicina (Kaunas, Lithuania) · 2021Review
- Integration of Molecular Information in Risk Assessment of Patients with Myeloproliferative Neoplasms.Cells · 2021Review
- Molecular pathogenesis of the myeloproliferative neoplasms.Journal of hematology & oncology · 2021Review
- PPARγ agonists promote the resolution of myelofibrosis in preclinical models.The Journal of clinical investigation · 2021Article
- The Role of Megakaryocytes in Myelofibrosis.Hematology/oncology clinics of North America · 2021Review
- Genome editing to model and reverse a prevalent mutation associated with myeloproliferative neoplasms.PloS one · 2021Article
- Clonal Hematopoiesis, Cardiovascular Diseases and Hematopoietic Stem Cells.International journal of molecular sciences · 2020Review
- Murine Models of Myelofibrosis.Cancers · 2020Review
- Review
- Givinostat: an emerging treatment for polycythemia vera.Expert opinion on investigational drugs · 2020Review
12 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The JAK2V617F mutation has been identified in most cases of Ph-negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). Expression of JAK2V617F results in constitutive activation of multiple signaling molecules/pathways. However, the key signaling downstream of JAK2V617F required for transformation and induction of MPNs remains elusive. Using a mouse genetic strategy, we show here that Stat5 is absolutely required for the pathogenesis of PV induced by Jak2V617F. Whereas expression of Jak2V617F in mice resulted in all the features of human PV, including an increase in red blood cells, hemoglobin, hematocrit, white blood cells, platelets, and splenomegaly, deletion of Stat5 in the Jak2V617F knockin mice normalized all the blood parameters and the spleen size. Furthermore, deletion of Stat5 completely abrogated erythropoietin (Epo)-independent erythroid colony formation evoked by Jak2V617F, a hallmark feature of PV. Re-expression of Stat5 in Stat5-deficient Jak2V617F knockin mice completely rescued the defects in transformation of hematopoietic progenitors and the PV phenotype. Together, these results indicate a critical function for Stat5 in the pathogenesis of PV. These findings also provide strong support for the development of Stat5 inhibitors as targeted therapies for the treatment of PV and other JAK2V617F-positive MPNs.
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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.