ArticleBlood2020
HDAC11 deficiency disrupts oncogene-induced hematopoiesis in myeloproliferative neoplasms.
Article in Blood, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
The trial behind it
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
35 citing papers in PubMed, 60 citations in OpenAlex.
- Structure-guided identification of histone deacetylase 11 inhibitors for targeted chemotherapy through long-timescale molecular dynamics simulation.Journal of molecular modeling · 2026Article
- HDAC11 as a potential therapeutic target for Alzheimer's disease.Drug discovery today · 2026Review
- Super-enhancer-associated lncRNA HDAC11-AS1 aggravates hepatocellular carcinoma progression by modulating HDAC11 and NUP210 expression via promoting super-enhancer activity.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Hdac11 promotes idiopathic pulmonary fibrosis through macrophage M2-type polarization and myofibroblast accumulation by inhibiting Parkin-dependent mitophagy.Nature communications · 2026Article
- Histone modifications in the regulation of erythropoiesis.Annals of medicine · 2025Review
- The deacetylases HDAC1/HDAC2 control JAK2Signal transduction and targeted therapy · 2025Article
- Review
- Epigenetic regulation of megakaryopoiesis and platelet formation.Haematologica · 2024Review
- SHP2 inhibition displays efficacy as a monotherapy and in combination with JAK2 inhibition in preclinical models of myeloproliferative neoplasms.American journal of hematology · 2024Article
- Transcriptional Expression of Histone Acetyltransferases and Deacetylases During the Recovery of Acute Exercise in Mouse Hippocampus.Journal of molecular neuroscience : MN · 2024Article
- Article
- Comparative Structure-Based Virtual Screening Utilizing Optimized AlphaFold Model Identifies Selective HDAC11 Inhibitor.International journal of molecular sciences · 2024Article
- FT895 Impairs Mitochondrial Function in Malignant Peripheral Nerve Sheath Tumor Cells.International journal of molecular sciences · 2023Article
- HDAC11 mediates the ubiquitin-dependent degradation of p53 and inhibits the anti-leukemia effect of PD0166285.Medical oncology (Northwood, London, England) · 2023Article
- Recent advances in therapies for primary myelofibrosis.Faculty reviews · 2023Review
- HDAC6 regulates human erythroid differentiation through modulation of JAK2 signalling.Journal of cellular and molecular medicine · 2023Article
- Histone Deacetylases Function in the Control of Early Hematopoiesis and Erythropoiesis.International journal of molecular sciences · 2022Review
- Epigenetic downregulation of Socs2 contributes to mutant N-Ras-mediated hematopoietic dysregulation.Disease models & mechanisms · 2022Article
- GM-CSF impairs erythropoiesis by disrupting erythroblastic island formation via macrophages.Journal of translational medicine · 2022Article
- Comprehensive Analysis of the Differential Expression and Prognostic Value of Histone Deacetylases in Glioma.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
31 authors at 8 institutions in 2 countries.
Funding
Abstract
Protein acetylation is an important contributor to cancer initiation. Histone deacetylase 6 (HDAC6) controls JAK2 translation and protein stability and has been implicated in JAK2-driven diseases best exemplified by myeloproliferative neoplasms (MPNs). By using novel classes of highly selective HDAC inhibitors and genetically deficient mouse models, we discovered that HDAC11 rather than HDAC6 is necessary for the proliferation and survival of oncogenic JAK2-driven MPN cells and patient samples. Notably, HDAC11 is variably expressed in primitive stem cells and is expressed largely upon lineage commitment. Although Hdac11is dispensable for normal homeostatic hematopoietic stem and progenitor cell differentiation based on chimeric bone marrow reconstitution, Hdac11 deficiency significantly reduced the abnormal megakaryocyte population, improved splenic architecture, reduced fibrosis, and increased survival in the MPLW515L-MPN mouse model during primary and secondary transplantation. Therefore, inhibitors of HDAC11 are an attractive therapy for treating patients with MPN. Although JAK2 inhibitor therapy provides substantial clinical benefit in MPN patients, the identification of alternative therapeutic targets is needed to reverse MPN pathogenesis and control malignant hematopoiesis. This study establishes HDAC11 as a unique type of target molecule that has therapeutic potential in MPN.
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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.