ArticleThe Journal of clinical investigation2018
Loss of pleckstrin-2 reverts lethality and vascular occlusions in JAK2V617F-positive myeloproliferative neoplasms.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Fufang Huangbo Formula mitigates myeloproliferative neoplasms by activating p53/p21 signaling axis and inhibiting STAT3 and NF-κB signaling pathways.Pharmaceutical science advances · 2026Article
- Spatial transcriptomic analyses highlight distinct erythroid niches in mice and humans.Nature genetics · 2026Article
- Stromal Gasdermin D-mediated Pyroptosis Drives Maladaptive CD4bioRxiv : the preprint server for biology · 2026Article
- Targeting DESI2 as a Novel Therapeutic Strategy for JAK2-Mutant Leukemias.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pleckstrin-2 promotes the progression of colorectal cancer via YTHDF2-mediated TYMS mRNA stability.Cellular and molecular life sciences : CMLS · 2025Article
- PPIL2 is a target of the JAK2/STAT5 pathway and promotes myeloproliferation via degradation of p53.The Journal of clinical investigation · 2025Article
- Molecular characterization underlying IFN-α2 treatment in polycythemia vera: a transcriptomic overview.Molecular and cellular biochemistry · 2025Article
- Development of iPSC-derived human bone marrow organoid for autonomous hematopoiesis and patient-derived HSPC engraftment.Blood advances · 2025Article
- Pleckstrin-2 Mediates the Activation of AKT in Prostate Cancer and Is Repressed by Androgen Receptor.The American journal of pathology · 2024Article
- Exacerbation of thromboinflammation by JAK2V617F mutation worsens the prognosis of cerebral venous sinus thrombosis.Blood advances · 2024Article
- Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms.Cancer discovery · 2024Article
- 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
- Article
- JAK2V617F mutation drives vascular resident macrophages toward a pathogenic phenotype and promotes dissecting aortic aneurysm.Nature communications · 2022Article
- Bone marrow-confined IL-6 signaling mediates the progression of myelodysplastic syndromes to acute myeloid leukemia.The Journal of clinical investigation · 2022Article
- PLEK2 promotes the proliferation and migration of non-small cell lung cancer cells in a BRD4-dependent manner.Molecular biology reports · 2022Article
- Clonal hematopoiesis in cardiovascular disease and therapeutic implications.Nature cardiovascular research · 2022Article
- Fine-Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Pleckstrin 2 is a potential drug target for colorectal carcinoma with activation of APC/β‑catenin.Molecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
V617F driver mutation of JAK2 is the leading cause of the Philadelphia-chromosome-negative myeloproliferative neoplasms (MPNs). Although thrombosis is a leading cause of mortality and morbidity in MPNs, the mechanisms underlying their pathogenesis are unclear. Here, we identified pleckstrin-2 (Plek2) as a downstream target of the JAK2/STAT5 pathway in erythroid and myeloid cells, and showed that it is upregulated in a JAK2V617F-positive MPN mouse model and in patients with MPNs. Loss of Plek2 ameliorated JAK2V617F-induced myeloproliferative phenotypes including erythrocytosis, neutrophilia, thrombocytosis, and splenomegaly, thereby reverting the widespread vascular occlusions and lethality in JAK2V617F-knockin mice. Additionally, we demonstrated that a reduction in red blood cell mass was the main contributing factor in the reversion of vascular occlusions. Thus, our study identifies Plek2 as an effector of the JAK2/STAT5 pathway and a key factor in the pathogenesis of JAK2V617F-induced MPNs, pointing to Plek2 as a viable target for the treatment of MPNs.
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