ArticleNeurochemical research2017
14-3-3 Isoforms Differentially Regulate NFκB Signaling in the Brain After Ischemia-Reperfusion.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- The mRNA and protein of IL-8 oppositely regulate PRRSV replication via nucleoprotein and 14-3-3γ.Journal of virology · 2025Article
- Comprehensive Review on Bimolecular Fluorescence Complementation and Its Application in Deciphering Protein-Protein Interactions in Cell Signaling Pathways.Biomolecules · 2024Review
- Monotropein Protects Mesenchymal Stem Cells from Lipopolysaccharide-Induced Impairments and Promotes Fracture Healing in an Ovariectomized Mouse Model.Calcified tissue international · 2023Article
- Protein-protein interactions: developing small-molecule inhibitors/stabilizers through covalent strategies.Trends in pharmacological sciences · 2023Review
- LncRNA SNHG7 Knockdown Aggravates Hepatic Ischemia-Reperfusion Injury and Promotes Apoptosis in Hemorrhagic Shock Pregnant Rats by Modulating miR-34a-5p/YWHAG Axis.Molecular biotechnology · 2023Article
- Identification of optimal reference genes for gene expression studies in a focal cerebral ischaemia model-Spatiotemporal effects.Journal of cellular and molecular medicine · 2022Article
- Article
- Nipah virus W protein harnesses nuclear 14-3-3 to inhibit NF-κB-induced proinflammatory response.Communications biology · 2021Article
- Identification and confirmation of 14-3-3 ζ as a novel target of ginsenosides in brain tissues.Journal of ginseng research · 2021Article
- An Exploration of Chemical Properties Required for Cooperative Stabilization of the 14-3-3 Interaction with NF-κB-Utilizing a Reversible Covalent Tethering Approach.Journal of medicinal chemistry · 2021Article
- Emerging roles of 14-3-3γ in the brain disorder.BMB reports · 2020Review
- Selectivity via Cooperativity: Preferential Stabilization of the p65/14-3-3 Interaction with Semisynthetic Natural Products.Journal of the American Chemical Society · 2020Article
- Selective 14-3-3γ Upregulation Promotes Beclin-1-LC3-Autophagic Influx via β-Catenin Interaction in Starved Neurons In Vitro and In Vivo.Neurochemical research · 2019Article
- Mass Spectrometry-Based Proteomic Profiling of Thrombotic Material Obtained by Endovascular Thrombectomy in Patients with Ischemic Stroke.International journal of molecular sciences · 2018Article
- Cellular stress and redox activity proteins are involved in gastric carcinogenesis associated with Helicobacter pylori infection expressing high levels of thioredoxin-1.Journal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian 14-3-3 isoforms exist predominantly in the brain and are heavily involved in neurological diseases. However, the isoform-specific role of 14-3-3 proteins in the brain remains largely unclear. Here, we investigated the role of 14-3-3 isoforms in rat brains after transient middle cerebral artery occlusion and reperfusion. 14-3-3β, η, γ and ζ but not ε or τ were selectively upregulated in cerebral cortical neurons after ischemia-reperfusion (I/R). Selectively, 14-3-3β, γ and ζ were translocated from cytoplasm into the nuclei of neurons after I/R. 14-3-3 bound to p65 and suppressed p65 expression in N2a cells. In the brain, 14-3-3 could either colocalize with p65 in the nuclei of neurons or segregate from p65 expression in cortical neurons after I/R. All evidence together suggests that 14-3-3 isoforms are differentially induced to enter into the nuclei of neurons after I/R, which might regulate NFκB signaling directly or indirectly. Since 14-3-3 proteins are essential for cell survival and NFκB is a key transcriptional factor, our data suggest that the 14-3-3/p65 signaling pathway might be a potential therapeutic target for stroke.
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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.