ArticleThe EMBO journal2003
Critical loss of CBP/p300 histone acetylase activity by caspase-6 during neurodegeneration.
Article in The EMBO journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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Who cites it
145 citing papers in PubMed, 299 citations in OpenAlex.
- Epigenetic Modulation Is a Key Mechanism in Cognitive Deficit: Unveiling Garcinol as a Potent HAT Inhibitor in Improving Alzheimer's Disease.ACS omega · 2026Review
- The Intricate Role of Caspase-6 and Death Receptor-6 in Neurodegenerative Diseases.Cell biochemistry and biophysics · 2026Review
- Microglial histone deacetylase-3 conditional deletion attenuates neurological deficits after intracerebral hemorrhage.Frontiers in cellular neuroscience · 2026Article
- Hematoma-driven immuno-epigenetic remodeling after intracerebral hemorrhage: cell-type-specific mechanisms and therapeutic opportunities.Frontiers in immunology · 2026Review
- Epigenetic Regulation in Ischemic Neuroprotection: The Dual Role of HDACs and HATs in Neuroinflammation and Recovery.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- The epigenetic potential of vitamin K2 in brain health.Epigenomics · 2025Review
- Review
- Mapping the hippocampal spatial proteomic signature in male and female mice of an early Alzheimer's disease model.Biology of sex differences · 2025Article
- Tip60 HAT activators as therapeutic modulators for Alzheimer's disease.Nature communications · 2025Article
- Exploring epigenetic modifications as potential biomarkers and therapeutic targets in amyotrophic lateral sclerosis.Journal of neurology · 2025Review
- Direct and Indirect Protein Interactions Link FUS Aggregation to Histone Post-Translational Modification Dysregulation and Growth Suppression in an ALS/FTD Yeast Model.Journal of fungi (Basel, Switzerland) · 2025Article
- Histone Deacetylase Inhibition in Alzheimer's Disease: Molecular Mechanisms, Therapeutic Potential, and Future Perspectives.Current topics in medicinal chemistry · 2025Review
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- ATXN3: a multifunctional protein involved in the polyglutamine disease spinocerebellar ataxia type 3.Expert reviews in molecular medicine · 2024Review
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- The evolution of small molecule enzyme activators.RSC medicinal chemistry · 2023Review
- Global profiling of ribosomal protein acetylation reveals essentiality of acetylation homeostasis in maintaining ribosome assembly and function.Nucleic acids research · 2023Article
- ATXN3 controls DNA replication and transcription by regulating chromatin structure.Nucleic acids research · 2023Article
- Protective effect of hydrogen sulfide is mediated by negative regulation of epigenetic histone acetylation in Parkinson's disease.Archives of medical science : AMS · 2023Article
85 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
By altering chromatin structure, histone acetyltransferases (HATs) act as transcriptional regulators. We observed in a model of primary neurons that histone acetylation levels decreased at the onset of apoptosis. The CREB-binding protein (CBP) is a HAT of particular interest because it also acts as a co-activator controlling, among others, CREB-dependent transcriptional activity. It has been demonstrated that CREB exerts neuroprotective functions, but the fate of CBP during neuronal apoptosis remained unclear till now. This work provided evidence that CBP is specifically targeted by caspases and calpains at the onset of neuronal apoptosis, and CBP was futher identified as a new caspase-6 substrate. This ultimately impinged on the CBP/p300 HAT activity that decreased with time during apoptosis entry, whereas total cellular HAT activity remained unchanged. Interestingly, CBP loss and histone deacetylation were observed in two different pathological contexts: amyloid precursor protein-dependent signaling and amyotrophic lateral sclerosis model mice, indicating that these modifications are likely to contribute to neurodegenerative diseases. In terms of function, we demonstrated that fine-tuning of CBP HAT activity is necessary to ensure neuroprotection.
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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.