ArticleNature communications2017
Critical role of the HDAC6-cortactin axis in human megakaryocyte maturation leading to a proplatelet-formation defect.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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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Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Selective targeting of cortactin tandem repeat acetylation by human lysine deacetylases.The FEBS journal · 2026Article
- Novel histone deacetylase inhibitor, CS014, attenuates in vivo thrombosis while maintaining hemostasis.Journal of thrombosis and haemostasis : JTH · 2026Article
- Targeted Degradation of Histone Deacetylase 8 Using Proteolysis Targeting Chimeras Technology: A Promising Approach for Glioblastoma Treatment.Drug design, development and therapy · 2026Article
- Proteomic Validation of MEG-01-Derived Extracellular Vesicles as Representative Models for Megakaryocyte- and Platelet-Derived Extracellular Vesicles.Biomolecules · 2025Article
- Epigenetic regulation of megakaryopoiesis and platelet formation.Haematologica · 2024Review
- HDAC inhibitors as pharmacological treatment for Duchenne muscular dystrophy: a discovery journey from bench to patients.Trends in molecular medicine · 2024Review
- HDAC6 regulates human erythroid differentiation through modulation of JAK2 signalling.Journal of cellular and molecular medicine · 2023Article
- Article
- Histone Deacetylases Function in the Control of Early Hematopoiesis and Erythropoiesis.International journal of molecular sciences · 2022Review
- Design, Synthesis, Bioactivity Evaluation, Crystal Structures, and In Silico Studies of New α-Amino Amide Derivatives as Potential Histone Deacetylase 6 Inhibitors.Molecules (Basel, Switzerland) · 2022Article
- Ricolinostat promotes the generation of megakaryocyte progenitors from human hematopoietic stem and progenitor cells.Stem cell research & therapy · 2022Article
- Article
- Unique Molecular Interaction with the Histone Deacetylase 6 Catalytic Tunnel: Crystallographic and Biological Characterization of a Model Chemotype.Journal of medicinal chemistry · 2021Article
- Hypermethylation ofCells · 2020Article
- ATAT1 regulates forebrain development and stress-induced tubulin hyperacetylation.Cellular and molecular life sciences : CMLS · 2019Article
- New insights into cytoskeletal remodeling during platelet production.Journal of thrombosis and haemostasis : JTH · 2019Review
- Compounds targeting class II histone deacetylases do not cause panHDACI-associated impairment of megakaryocyte differentiation.Experimental hematology · 2019Article
- An essential role for α4A-tubulin in platelet biogenesis.Life science alliance · 2019Article
- Quantitative Proteomic Analysis Reveals the Sites Related to Acetylation and Mechanism of ACY-1215 in Acute Liver Failure Mice.Frontiers in pharmacology · 2019Article
- Silencing of HDAC6 as a therapeutic target in chronic lymphocytic leukemia.Blood advances · 2018Article
Corrections and comments
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Authors and funding
22 authors at 7 institutions in 3 countries.
Funding
Abstract
Thrombocytopenia is a major side effect of a new class of anticancer agents that target histone deacetylase (HDAC). Their mechanism is poorly understood. Here, we show that HDAC6 inhibition and genetic knockdown lead to a strong decrease in human proplatelet formation (PPF). Unexpectedly, HDAC6 inhibition-induced tubulin hyperacetylation has no effect on PPF. The PPF decrease induced by HDAC6 inhibition is related to cortactin (CTTN) hyperacetylation associated with actin disorganization inducing important changes in the distribution of megakaryocyte (MK) organelles. CTTN silencing in human MKs phenocopies HDAC6 inactivation and knockdown leads to a strong PPF defect. This is rescued by forced expression of a deacetylated CTTN mimetic. Unexpectedly, unlike human-derived MKs, HDAC6 and CTTN are shown to be dispensable for mouse PPF in vitro and platelet production in vivo. Our results highlight an unexpected function of HDAC6-CTTN axis as a positive regulator of human but not mouse MK maturation.
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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.