ArticleScience advances2020
The Huntingtin-interacting protein SETD2/HYPB is an actin lysine methyltransferase.
Article in Science advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 50 citations in OpenAlex.
- Nuclear activities and interactome of the NS5 protein of tick-borne encephalitis virus.Journal of virology · 2026Article
- Antagonistic roles of histone H3 lysine methyltransferases dictate tumor immune surveillance.Nature communications · 2026Article
- Dual apical methyltransferases orchestrate motility initiation in apicomplexan parasites.Nature communications · 2026Article
- Blocking SETD2 Enhances the Therapeutic Efficiency of Menin Inhibitor in MLL-Fusion Leukemia.Cancer science · 2026Article
- Beyond The Nucleus: Translating Engineered Protein Localization To Chromatin Modifying Enzymes.Current opinion in biomedical engineering · 2026Article
- Article
- The SETD2 L1609P mutation found in leukemia disrupts methyltransferase activity and reduces histone H3K36 trimethylation.The Journal of biological chemistry · 2026Article
- Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Characterization of Lysine Methylation During Neuronal Differentiation of LUHMES cells.bioRxiv : the preprint server for biology · 2026Article
- The emerging paradigms of SETD family enzymes as epigenetic regulators of the immune response in inflammatory diseases.Frontiers in immunology · 2026Review
- Emerging role of SETD2 in the development and function of immune cells.Genes & diseases · 2025Review
- Epigenetic Mechanisms Shaping Spine Regulation: Unveiling the Role of Cytoskeletal Dynamics and Localized Protein Synthesis.Molecular neurobiology · 2025Review
- KDM4A serves as an α-tubulin demethylase regulating microtubule polymerization and cell mitosis.Science advances · 2025Article
- Structure of the Huntingtin F-actin complex reveals its role in cytoskeleton organization.Science advances · 2025Article
- Mapping the genetic landscape of iron metabolism uncovers the SETD2 methyltransferase as a modulator of iron flux.Science advances · 2025Article
- Loss of SETD2 in wild-type VHL clear cell renal cell carcinoma sensitizes cells to STF-62247 and leads to DNA damage, cell cycle arrest, and cell death characteristic of pyroptosis.Molecular oncology · 2025Article
- Chromatin modifiers in neurodevelopment.Frontiers in molecular neuroscience · 2025Review
- Catalytic activity of Setd2 is essential for embryonic development in mice: establishment of a mouse model harboring patient-derived Setd2 mutation.Frontiers of medicine · 2024Article
- The histone methyltransferase SETD2 regulates HIV expression and latency.PLoS pathogens · 2024Article
- Lysine Methyltransferase EhPKMT2 Is Involved in the In Vitro Virulence ofPathogens (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 1 country.
Funding
Abstract
The methyltransferase SET domain-containing 2 (SETD2) was originally identified as Huntingtin (HTT) yeast partner B. However, a SETD2 function associated with the HTT scaffolding protein has not been elucidated, and no linkage between HTT and methylation has yet been uncovered. Here, we show that SETD2 is an actin methyltransferase that trimethylates lysine-68 (ActK68me3) in cells via its interaction with HTT and the actin-binding adapter HIP1R. ActK68me3 localizes primarily to the insoluble F-actin cytoskeleton in cells and regulates actin polymerization/depolymerization dynamics. Disruption of the SETD2-HTT-HIP1R axis inhibits actin methylation, causes defects in actin polymerization, and impairs cell migration. Together, these data identify SETD2 as a previously unknown HTT effector regulating methylation and polymerization of actin filaments and provide new avenues for understanding how defects in SETD2 and HTT drive disease via aberrant cytoskeletal methylation.
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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.