ArticleThe Journal of biological chemistry2009
Phosphorylation of neuronal survival factor MEF2D by glycogen synthase kinase 3beta in neuronal apoptosis.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 56 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Article
- Tetramethylpyrazine nitrone exerts neuroprotection via activation of PGC-1α/Nrf2 pathway in Parkinson's disease models.Journal of advanced research · 2024Article
- The Role of MEF2 Transcription Factor Family in Neuronal Survival and Degeneration.International journal of molecular sciences · 2023Review
- Identification of a Novel Small RNA Encoded in the Mouse Urokinase Receptor uPAR Gene (Frontiers in molecular neuroscience · 2022Article
- Sex-specific transcriptional rewiring in the brain of Alzheimer's disease patients.Frontiers in aging neuroscience · 2022Article
- Serum Metabolomics of Benign Essential Blepharospasm Using Liquid Chromatography and Orbitrap Mass Spectrometry.Oxidative medicine and cellular longevity · 2022Article
- Involvement of myocyte enhancer factor 2c in the pathogenesis of autism spectrum disorder.Heliyon · 2021Review
- Regulation of IFN-Is by MEF2D Promotes Inflammatory Homeostasis in Microglia.Journal of inflammation research · 2021Article
- Article
- Serum Metabolomics of Early Postoperative Cognitive Dysfunction in Elderly Patients Using Liquid Chromatography and Q-TOF Mass Spectrometry.Oxidative medicine and cellular longevity · 2020Article
- MEF2 transcription factors differentially contribute to retinal ganglion cell loss after optic nerve injury.PloS one · 2020Article
- MEF-2 isoforms' (A-D) roles in development and tumorigenesis.Oncotarget · 2019Review
- Pathogenic Feed-Forward Mechanisms in Alzheimer's and Parkinson's Disease Converge on GSK-3.Brain plasticity (Amsterdam, Netherlands) · 2018Review
- Neuroprotection Against MPPFrontiers in pharmacology · 2018Article
- GSK-3 Inhibitors and Tooth Repair: An Ethical Analysis.Frontiers in pharmacology · 2018Review
- Molecular Pathways: Revisiting Glycogen Synthase Kinase-3β as a Target for the Treatment of Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2017Review
- MEF2D Mediates the Neuroprotective Effect of Methylene Blue Against Glutamate-Induced Oxidative Damage in HT22 Hippocampal Cells.Molecular neurobiology · 2017Article
- The potential role of neuroinflammation and transcription factors in Parkinson disease.Dialogues in clinical neuroscience · 2017Review
- FMRP-dependent Mdm2 dephosphorylation is required for MEF2-induced synapse elimination.Human molecular genetics · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glycogen synthase kinase 3beta (GSK3beta) has been identified to play important roles in neuronal death. Evidence from both in vitro and in vivo studies indicates that increased GSK3beta activity contributes to neurodegeneration and to the pathogenesis of Alzheimer disease. But the molecular mechanisms that underlie GSK3beta-mediated neurotoxicity remain poorly understood. We reported here that myocyte enhancer factor 2D (MEF2D), a nuclear transcription factor known to promote neuronal survival, is directly phosphorylated by GSK3beta. Our data showed that phosphorylation of MEF2D by GSK3beta at three specific residues in its transactivation domain inhibits MEF2D transcriptional activity. Withdrawal of neuronal activity in cerebellar granule neurons activated GSK3beta in the nucleus, leading to GSK3beta-dependent inhibition of MEF2 function. This inhibition contributed to GSK3beta-mediated neuronal toxicity. Overexpression of MEF2D mutant that is resistant to GSK3beta inhibition protected cerebellar granule neurons from either GSK3beta activation- or neuronal activity deprivation-induced toxicity. These results identify survival factor MEF2D as a novel downstream effector targeted by GSK3beta and define a molecular link between activation of GSK3beta and neuronal survival machinery which may underlie in part GSK3beta-mediated neurotoxicity.
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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.