ArticleNature neuroscience2010
HDAC1 nuclear export induced by pathological conditions is essential for the onset of axonal damage.
Article in Nature neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03092544 (Investigating Indirect Mechanism of Neuroprotection of Tecfidera®), which is not on this map. Cited by 129 papers, 1 of them a synthesis that pooled it.
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.
Investigating Indirect Mechanism of Neuroprotection of Tecfidera® (Dimethyl Fumarate) in RRMS and Progressive Patients
Who cites it
129 citing papers in PubMed, 1 synthesis or guideline pooled it, 208 citations in OpenAlex.
- Benefits of histone deacetylase inhibitors for acute brain injury: a systematic review of animal studies.Journal of neurochemistry · 2010Pooled it
- Insights into neuroepigenetics through human histone deacetylase PET imaging.Science translational medicine · 2016Trial
- Propionic acid in multiple sclerosis: a phase 2b, double-blind, randomized placebo-controlled trial.Brain : a journal of neurology · 2026Article
- GFI1 enhances MHC-I expression in tumor cells and augments tumor responsiveness to PD-1/PD-L1 inhibitors.Cancer immunology, immunotherapy : CII · 2026Article
- Histone Deacetylase 2 in Alzheimer's Disease: A Comprehensive Molecular Blueprint for Therapeutic Targeting.Molecular neurobiology · 2025Review
- Unlocking therapeutic potential in traumatic brain injury: exploring microenvironmental targets, signaling pathways and translational hurdles.Inflammopharmacology · 2025Review
- Is SIRT3 and Mitochondria a Reliable Target for Parkinson's Disease and Aging? A Narrative Review.Molecular neurobiology · 2025Review
- Potential therapeutic targets for ischemic stroke in pre-clinical studies: Epigenetic-modifying enzymes DNMT/TET and HAT/HDAC.Frontiers in pharmacology · 2025Review
- Abnormal cytoskeletal remodeling but normal neuronal excitability in a mouse model of the recurrent developmental and epileptic encephalopathy-susceptibility KCNB1-p.R312H variant.Communications biology · 2024Article
- ELM2-SANT Domain-Containing Scaffolding Protein 1 Regulates Differentiation and Maturation of Cardiomyocytes Derived From Human-Induced Pluripotent Stem Cells.Journal of the American Heart Association · 2024Article
- Cell-type specific circadian transcription factor BMAL1 roles in excitotoxic hippocampal lesions to enhance neurogenesis.iScience · 2024Article
- Propionic acid promotes neurite recovery in damaged multiple sclerosis neurons.Brain communications · 2024Article
- Transcriptional mutagenesis of α-synuclein caused by DNA oxidation in Parkinson's disease pathogenesis.Acta neuropathologica · 2023Article
- The role of HDAC3 and its inhibitors in regulation of oxidative stress and chronic diseases.Cell death discovery · 2023Review
- Trait - driven analysis of the 2p15p16.1 microdeletion syndrome suggests a complex pattern of interactions between candidate genes.Genes & genomics · 2023Article
- Tau-dependent HDAC1 nuclear reduction is associated with altered VGluT1 expression.Frontiers in cell and developmental biology · 2023Article
- HDAC1 is Involved in Neuroinflammation and Blood-Brain Barrier Damage in Stroke Pathogenesis.Journal of inflammation research · 2023Article
- Review
- Bacterial neurotoxic metabolites in multiple sclerosis cerebrospinal fluid and plasma.Brain : a journal of neurology · 2022Article
- Restoration of HDAC1 Enzymatic Activity after Stroke Protects Neurons from Ischemia/Reperfusion Damage and Attenuates Behavioral Deficits in Rats.International journal of molecular sciences · 2021Article
69 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Histone deacetylase 1 (HDAC1) is a nuclear enzyme involved in transcriptional repression. We detected cytosolic HDAC1 in damaged axons in brains of humans with multiple sclerosis and of mice with cuprizone-induced demyelination, in ex vivo models of demyelination and in cultured neurons exposed to glutamate and tumor necrosis factor-alpha. Nuclear export of HDAC1 was mediated by the interaction with the nuclear receptor CRM-1 and led to impaired mitochondrial transport. The formation of complexes between exported HDAC1 and members of the kinesin family of motor proteins hindered the interaction with cargo molecules, thereby inhibiting mitochondrial movement and inducing localized beading. This effect was prevented by inhibiting HDAC1 nuclear export with leptomycin B, treating neurons with pharmacological inhibitors of HDAC activity or silencing HDAC1 but not other HDAC isoforms. Together these data identify nuclear export of HDAC1 as a critical event for impaired mitochondrial transport in damaged neurons.
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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.