ArticleThe Journal of biological chemistry2011
Neuroprotection by histone deacetylase-7 (HDAC7) occurs by inhibition of c-jun expression through a deacetylase-independent mechanism.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
- Targeting Histone Deacetylase 2 in Alzheimer's Disease: From Molecular Insights to Epigenetic Therapeutic Opportunities.Molecular neurobiology · 2026Review
- Cell-type-specific architecture of the hypothalamus in a socially plastic vertebrate.bioRxiv : the preprint server for biology · 2026Article
- Defining the heterogeneous molecular landscape of lung cancer cell responses to epigenetic inhibition.Communications biology · 2026Article
- Epigenetic Dysregulation in Neurodegeneration: The Role of Histone Deacetylases and Emerging Inhibitor Strategies.Biomolecules · 2026Review
- Dose-Dependent Effects of Myo-Inositol on Kainic Acid-Induced Epilepsy: Electrophysiological, Behavioral, Transcriptomic, and DNA Methylome Studies.International journal of molecular sciences · 2025Article
- Histone deacetylase 7 mediates lipopolysaccharide-inducible mitochondrial fission in macrophages.Journal of cell science · 2025Article
- Scaffolding Activities of Pseudodeacetylase HDAC7.ACS chemical biology · 2025Review
- Genetic and epigenetic targets of natural dietary compounds as anti-Alzheimer's agents.Neural regeneration research · 2024Review
- Unlocking the epigenetic symphony: histone acetylation's impact on neurobehavioral change in neurodegenerative disorders.Epigenomics · 2024Review
- Histone deacetylase 7: a signalling hub controlling development, inflammation, metabolism and disease.The FEBS journal · 2023Review
- A Role for Histone Deacetylases in the Biology and Treatment of Post-Traumatic Stress Disorder: What Do We Know and Where Do We Go from Here?Complex psychiatry · 2022Review
- Sex Differences in Psychostimulant Abuse: Implications for Estrogen Receptors and Histone Deacetylases.Genes · 2022Review
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- KLF2 up-regulates IRF4/HDAC7 to protect neonatal rats from hypoxic-ischemic brain damage.Cell death discovery · 2022Article
- The role of altered protein acetylation in neurodegenerative disease.Frontiers in aging neuroscience · 2022Review
- Understanding the Role of Histone Deacetylase and their Inhibitors in Neurodegenerative Disorders: Current Targets and Future Perspective.Current neuropharmacology · 2022Review
- A Glossary for Chemical Approaches towards Unlocking the Trove of Metabolic Treasures inMolecules (Basel, Switzerland) · 2021Review
- Opportunities for histone deacetylase inhibition in amyotrophic lateral sclerosis.British journal of pharmacology · 2021Review
- Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat.Cancer drug resistance (Alhambra, Calif.) · 2021Article
- OIP5-AS1 modulates epigenetic regulator HDAC7 to enhance non-small cell lung cancer metastasis via miR-140-5p.Oncology letters · 2020Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase (HDAC) 7 is a member of the HDAC family of deacetylases. Although some of the HDAC proteins have been shown to regulate neuronal survival and death, whether HDAC7 has a similar role is not known. In this study, we show that HDAC7 protects neurons from apoptosis. In cerebellar granule neurons (CGNs) primed to undergo apoptosis by low potassium treatment, expression of HDAC7 protein is reduced. Reduced expression is also observed in CGNs induced to die by pharmacological inhibition of the proteasome, in cortical neurons treated with homocysteic acid, and in the striatum of R6/2 transgenic mice, a commonly used genetic model of Huntington disease. Forced expression of HDAC7 in cultured CGNs blocks low potassium-induced death, and shRNA-mediated suppression of its expression induces death in otherwise healthy neurons. HDAC7-mediated neuroprotection does not require its catalytic domain and cannot be inhibited by chemical inhibitors of HDACs. Moreover, pharmacological inhibitors of the PI3K-Akt or Raf-MEK-ERK signaling pathways or that of PKA, PKC, and Ca(2+)/calmodulin-dependent protein kinase fail to reduce neuroprotection by HDAC7. We show that stimulation of c-jun expression, an essential feature of neuronal death, is prevented by HDAC7. shRNA-mediated suppression of HDAC7 expression leads to an increase in c-jun expression. Inhibition of c-jun expression by HDAC7 is mediated at the transcriptional level by its direct association with the c-jun gene promoter. Taken together, our results indicate that HDAC7 is a neuroprotective protein acting by a mechanism that is independent of its deacetylase activity but involving the inhibition of c-jun expression.
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