ArticleMolecular and cellular neurosciences2014
The histone lysine demethylase Kdm6b is required for activity-dependent preconditioning of hippocampal neuronal survival.
Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Inhibition of Astrocytic JMJD3 Attenuates Neuroinflammation-Mediated Blood-Brain Barrier Disruption and Improves Functional Recovery After Intracerebral Hemorrhage in Mice.Brain sciences · 2026Article
- Histone demethylase KDM6B promotes postnatal oligodendrocyte maturation and cortical myelination.Frontiers in cellular neuroscience · 2026Article
- Roles of Kdm6a and Kdm6b in Regulation of Mammalian Neural Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Impact of KDM6B mosaic brain knockout on synaptic function and behavior.Scientific reports · 2024Article
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- Dysregulation of the histone demethylase KDM6B in alcohol dependence is associated with epigenetic regulation of inflammatory signaling pathways.Addiction biology · 2021Article
- Mantis-ml: Disease-Agnostic Gene Prioritization from High-Throughput Genomic Screens by Stochastic Semi-supervised Learning.American journal of human genetics · 2020Article
- Histone demethylases in neuronal differentiation, plasticity, and disease.Current opinion in neurobiology · 2019Review
- Kdm6b regulates context-dependent hematopoietic stem cell self-renewal and leukemogenesis.Leukemia · 2019Article
- A novel environment-evoked transcriptional signature predicts reactivity in single dentate granule neurons.Nature communications · 2018Article
- Long genes linked to autism spectrum disorders harbor broad enhancer-like chromatin domains.Genome research · 2018Article
- The histone demethylase Kdm6b regulates a mature gene expression program in differentiating cerebellar granule neurons.Molecular and cellular neurosciences · 2018Review
- Cocaine Administration and Its Withdrawal Enhance the Expression of Genes Encoding Histone-Modifying Enzymes and Histone Acetylation in the Rat Prefrontal Cortex.Neurotoxicity research · 2017Article
- Review
- Activity-Dependent Degradation of Synaptic Vesicle Proteins Requires Rab35 and the ESCRT Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Kdm6b and Pmepa1 as Targets of Bioelectrically and Behaviorally Induced Activin A Signaling.Molecular neurobiology · 2016Article
- Alcohol-induced suppression of KDM6B dysregulates the mineralization potential in dental pulp stem cells.Stem cell research · 2016Article
- The transcription factor calcium-response factor limits NMDA receptor-dependent transcription in the developing brain.Journal of neurochemistry · 2016Article
- Definition of a Bidirectional Activity-Dependent Pathway Involving BDNF and Narp.Cell reports · 2015Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Enzymes that regulate histone lysine methylation play important roles in neuronal differentiation, but little is known about their contributions to activity-regulated gene transcription in differentiated neurons. We characterized activity-regulated expression of lysine demethylases and lysine methyltransferases in the hippocampus of adult male mice following pilocarpine-induced seizure. Pilocarpine drove a 20-fold increase in mRNA encoding the histone H3 lysine 27-specific demethylase Kdm6b selectively in granule neurons of the dentate gyrus, and this induction was recapitulated in cultured hippocampal neurons by bicuculline and 4-aminopyridine (Bic + 4AP) stimulation of synaptic activity. Because activity-regulated gene expression is highly correlated with neuronal survival, we tested the requirement for Kdm6b expression in Bic + 4AP induced preconditioning of neuronal survival. Prior exposure to Bic + 4AP promoted neuronal survival in control neurons upon growth factor withdrawal; however, this effect was ablated when we knocked down Kdm6b expression. Loss of Kdm6b did not disrupt activity-induced expression of most genes, including that of a gene set previously established to promote neuronal survival in this assay. However, using bioinformatic analysis of RNA sequencing data, we discovered that Kdm6b knockdown neurons showed impaired inducibility of a discrete set of genes annotated for their function in inflammation. These data reveal a novel function for Kdm6b in activity-regulated neuronal survival, and they suggest that activity- and Kdm6b-dependent regulation of inflammatory gene pathways may serve as an adaptive pro-survival response to increased neuronal activity.
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