ArticlePloS one2013
Transgenic overexpression of 14-3-3 zeta protects hippocampus against endoplasmic reticulum stress and status epilepticus in vivo.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 47 citations in OpenAlex.
- Disruption of electrophysiological rhythms and memory impairment in an Alzheimer's transgenic rat model.Alzheimer's research & therapy · 2025Article
- Preventing epileptogenesis by interaction between inositol isomers and proteins.Epilepsia open · 2025Article
- Modulation of Heme-Induced Inflammation Using MicroRNA-Loaded Liposomes: Implications for Hemolytic Disorders Such as Malaria and Sickle Cell Disease.International journal of molecular sciences · 2023Article
- The apple 14-3-3 geneFrontiers in plant science · 2023Article
- IRE1α RIDD activity induced under ER stress drives neuronal death by the degradation of 14-3-3 θ mRNA in cortical neurons during glucose deprivation.Cell death discovery · 2021Article
- The Dose-Dependent Pleiotropic Effects of the UBBFrontiers in molecular biosciences · 2021Review
- Downregulation of 14-3-3 Proteins in Alzheimer's Disease.Molecular neurobiology · 2020Article
- Redox proteomics and amyloid β-peptide: insights into Alzheimer disease.Journal of neurochemistry · 2019Review
- Context-Specific Switch from Anti- to Pro-epileptogenic Function of the P2YThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- TrkB-Shc Signaling Protects against Hippocampal Injury Following Status Epilepticus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- 14-3-3ζ protein protects against brain ischemia/reperfusion injury and induces BDNF transcription after MCAO in rat.Journal of applied biomedicine · 2019Article
- Tau Phosphorylation in a Mouse Model of Temporal Lobe Epilepsy.Frontiers in aging neuroscience · 2019Article
- Protein-protein interactions reveal key canonical pathways, upstream regulators, interactome domains, and novel targets in ALS.Scientific reports · 2018Article
- Molecular Cloning and Effects ofGenes · 2018Article
- Downregulation of 14-3-3 Proteins in a Kainic Acid-Induced Neurotoxicity Model.Molecular neurobiology · 2018Article
- γ2 GABAFrontiers in cellular neuroscience · 2018Review
- Spatiotemporal progression of ubiquitin-proteasome system inhibition after status epilepticus suggests protective adaptation against hippocampal injury.Molecular neurodegeneration · 2017Article
- Bottom-up proteomics analysis of the secretome of murine islets of Langerhans in elevated glucose levels.The Analyst · 2017Article
- Posttranscriptional regulation of 14-3-3ζ by RNA-binding protein HuR modulating intestinal epithelial restitution after wounding.Physiological reports · 2016Article
- Identification of Novel 14-3-3 Residues That Are Critical for Isoform-specific Interaction with GluN2C to Regulate N-Methyl-D-aspartate (NMDA) Receptor Trafficking.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
14-3-3 proteins are ubiquitous molecular chaperones that are abundantly expressed in the brain where they regulate cell functions including metabolism, the cell cycle and apoptosis. Brain levels of several 14-3-3 isoforms are altered in diseases of the nervous system, including epilepsy. The 14-3-3 zeta (ζ) isoform has been linked to endoplasmic reticulum (ER) function in neurons, with reduced levels provoking ER stress and increasing vulnerability to excitotoxic injury. Here we report that transgenic overexpression of 14-3-3ζ in mice results in selective changes to the unfolded protein response pathway in the hippocampus, including down-regulation of glucose-regulated proteins 78 and 94, activating transcription factors 4 and 6, and Xbp1 splicing. No differences were found between wild-type mice and transgenic mice for levels of other 14-3-3 isoforms or various other 14-3-3 binding proteins. 14-3-3ζ overexpressing mice were potently protected against cell death caused by intracerebroventricular injection of the ER stressor tunicamycin. 14-3-3ζ overexpressing mice were also potently protected against neuronal death caused by prolonged seizures. These studies demonstrate that increased 14-3-3ζ levels protect against ER stress and seizure-damage despite down-regulation of the unfolded protein response. Delivery of 14-3-3ζ may protect against pathologic changes resulting from prolonged or repeated seizures or where injuries provoke ER stress.
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