ArticleAntioxidants & redox signaling2011
Neuronal activity controls the antagonistic balance between peroxisome proliferator-activated receptor-γ coactivator-1α and silencing mediator of retinoic acid and thyroid hormone receptors in regulating antioxidant defenses.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- A postnatal molecular switch drives activity-dependent maturation of parvalbumin interneurons.Cell · 2025Article
- Nuclear receptor corepressor 1 levels differentially impact the intracellular dynamics of mutant thyroid hormone receptors associated with resistance to thyroid hormone syndrome.Molecular and cellular endocrinology · 2024Article
- Synaptic Activity Regulates Mitochondrial Iron Metabolism to Enhance Neuronal Bioenergetics.International journal of molecular sciences · 2023Article
- Mediator subunit MED1 modulates intranuclear dynamics of the thyroid hormone receptor.Journal of cellular biochemistry · 2020Article
- Neuronal Activity and Its Role in Controlling Antioxidant Genes.International journal of molecular sciences · 2020Review
- Thyroid hormone receptor localization in target tissues.The Journal of endocrinology · 2018Review
- Multiple exportins influence thyroid hormone receptor localization.Molecular and cellular endocrinology · 2015Article
- Mitochondrial fragmentation in excitotoxicity requires ROCK activation.Cell cycle (Georgetown, Tex.) · 2015Article
- Developmental and activity-dependent expression of LanCL1 confers antioxidant activity required for neuronal survival.Developmental cell · 2014Article
- SMRT-mediated co-shuttling enables export of class IIa HDACs independent of their CaM kinase phosphorylation sites.Journal of neurochemistry · 2013Article
- PGC-1α negatively regulates extrasynaptic NMDAR activity and excitotoxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Transcriptional Regulation by Nuclear Corepressors and PGC-1α: Implications for Mitochondrial Quality Control and Insulin Sensitivity.PPAR research · 2012Article
- Pituitary adenylate cyclase-activating peptide induces long-lasting neuroprotection through the induction of activity-dependent signaling via the cyclic AMP response element-binding protein-regulated transcription co-activator 1.Journal of neurochemistry · 2011Article
- Mechanisms of specificity in neuronal activity-regulated gene transcription.Progress in neurobiology · 2011Review
- The influence of synaptic activity on neuronal health.Current opinion in neurobiology · 2011Review
- Article
- Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders.Nature reviews. Neuroscience · 2010Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transcriptional coactivators and corepressors often have multiple targets and can have opposing actions on transcription and downstream physiological events. The coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is under-expressed in Huntington's disease and is a regulator of antioxidant defenses and mitochondrial biogenesis. We show that in primary cortical neurons, expression of PGC-1α strongly promotes resistance to excitotoxic and oxidative stress in a cell autonomous manner, whereas knockdown increases sensitivity. In contrast, the transcriptional corepressor silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) specifically antagonizes PGC-1α-mediated antioxidant effects. The antagonistic balance between PGC-1α and SMRT is upset in favor of PGC-1α by synaptic activity. Synaptic activity triggers nuclear export of SMRT reliant on multiple regions of the protein. Concomitantly, synaptic activity post-translationally enhances the transactivating potential of PGC-1α in a p38-dependent manner, as well as upregulating cyclic-AMP response element binding protein-dependent PGC-1α transcription. Activity-dependent targeting of PGC-1α results in enhanced gene expression mediated by the thyroid hormone receptor, a prototypical transcription factor coactivated by PGC-1α and repressed by SMRT. As a consequence of these events, SMRT is unable to antagonize PGC-1α-mediated resistance to oxidative stress in synaptically active neurons. Thus, PGC-1α and SMRT are antagonistic regulators of neuronal vulnerability to oxidative stress. Further, this coactivator-corepressor antagonism is regulated by the activity status of the cell, with implications for neuronal viability.
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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.