ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022
CBP Is Required for Establishing Adaptive Gene Programs in the Adult Mouse Brain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 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
- Cell type-specific functions of the PBAF chromatin-remodeling complex in neuronal diversification.Nature communications · 2025Article
- Genetic Mechanisms of Experience-Dependent Neuronal Plasticity.Annual review of genetics · 2025Review
- DNA glycosylases Ogg1 and Mutyh influence gene expression of PRC2 targets associated with cognition.Cellular and molecular life sciences : CMLS · 2025Article
- The omics era: a nexus of untapped potential for Mendelian chromatinopathies.Human genetics · 2024Review
- Maintenance of neuronal identity in C. elegans and beyond: Lessons from transcription and chromatin factors.Seminars in cell & developmental biology · 2024Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
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Abstract
Environmental factors and life experiences impinge on brain circuits triggering adaptive changes. Epigenetic regulators contribute to this neuroadaptation by enhancing or suppressing specific gene programs. The paralogous transcriptional coactivators and lysine acetyltransferases CREB binding protein (CBP) and p300 are involved in brain plasticity and stimulus-dependent transcription, but their specific roles in neuroadaptation are not fully understood. Here we investigated the impact of eliminating either CBP or p300 in excitatory neurons of the adult forebrain of mice from both sexes using inducible and cell type-restricted knock-out strains. The elimination of CBP, but not p300, reduced the expression and chromatin acetylation of plasticity genes, dampened activity-driven transcription, and caused memory deficits. The defects became more prominent in elderly mice and in paradigms that involved enduring changes in transcription, such as kindling and environmental enrichment, in which CBP loss interfered with the establishment of activity-induced transcriptional and epigenetic changes in response to stimulus or experience. These findings further strengthen the link between CBP deficiency in excitatory neurons and etiopathology in the nervous system.
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