ArticleJournal of neurochemistry2009
Protein kinase C regulation of neuronal zinc signaling mediates survival during preconditioning.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
The trial behind it
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
26 citing papers in PubMed, 65 citations in OpenAlex.
- Copper induces neuron-sparing, ferredoxin 1-independent astrocyte toxicity mediated by oxidative stress.Journal of neurochemistry · 2023Article
- The ZIP3 Zinc Transporter Is Localized to Mossy Fiber Terminals and Is Required for Kainate-Induced Degeneration of CA3 Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Protective Effects of Zinc on Spinal Cord Injury.Journal of molecular neuroscience : MN · 2021Review
- The Function and Regulation of Zinc in the Brain.Neuroscience · 2021Review
- The Redox Biology of Excitotoxic Processes: The NMDA Receptor, TOPA Quinone, and the Oxidative Liberation of Intracellular Zinc.Frontiers in neuroscience · 2020Review
- Critical Role of Zinc as Either an Antioxidant or a Prooxidant in Cellular Systems.Oxidative medicine and cellular longevity · 2018Review
- Disruption of KNeuroscience · 2017Article
- Targeting a Potassium Channel/Syntaxin Interaction Ameliorates Cell Death in Ischemic Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Molecular Mechanism of Disease-Associated Mutations in the Pre-M1 Helix of NMDA Receptors and Potential Rescue Pharmacology.PLoS genetics · 2017Article
- GRIN2D Recurrent De Novo Dominant Mutation Causes a Severe Epileptic Encephalopathy Treatable with NMDA Receptor Channel Blockers.American journal of human genetics · 2016Article
- Zn(2+) -induced Ca(2+) release via ryanodine receptors triggers calcineurin-dependent redistribution of cortical neuronal Kv2.1 K(+) channels.The Journal of physiology · 2016Article
- Zinc wave during the treatment of hypoxia is required for initial reactive oxygen species activation in mitochondria.International journal of physiology, pathophysiology and pharmacology · 2016Article
- Prophylactic Subacute Administration of Zinc Increases CCL2, CCR2, FGF2, and IGF-1 Expression and Prevents the Long-Term Memory Loss in a Rat Model of Cerebral Hypoxia-Ischemia.Neural plasticity · 2015Article
- Cyclin e1 regulates Kv2.1 channel phosphorylation and localization in neuronal ischemia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Voltage-gated potassium channels at the crossroads of neuronal function, ischemic tolerance, and neurodegeneration.Translational stroke research · 2014Review
- The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
- Intracellular Zn2+ accumulation enhances suppression of synaptic activity following spreading depolarization.Journal of neurochemistry · 2013Article
- A critical role for increased labile zinc in reducing sensitivity of cultured sheep pulmonary artery endothelial cells to LPS-induced apoptosis.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Redox regulation of intracellular zinc: molecular signaling in the life and death of neurons.Antioxidants & redox signaling · 2011Review
- Redox biochemistry of mammalian metallothioneins.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2011Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Sub-lethal activation of cell death processes initiate pro-survival signaling cascades. As intracellular Zn(2+) liberation mediates neuronal death pathways, we tested whether a sub-lethal increase in free Zn(2+) could also trigger neuroprotection. Neuronal free Zn(2+) transiently increased following preconditioning, and was both necessary and sufficient for conferring excitotoxic tolerance. Lethal exposure to NMDA led to a delayed increase in Zn(2+) that contributed significantly to excitotoxicity in non-preconditioned neurons, but not in tolerant neurons, unless preconditioning-induced free Zn(2+) was chelated. Thus, preconditioning may trigger the expression of Zn(2+)-regulating processes, which, in turn, prevent subsequent Zn(2+)-mediated toxicity. Indeed, preconditioning increased Zn(2+)-regulated gene expression in neurons. Examination of the molecular signaling mechanism leading to this early Zn(2+) signal revealed a critical role for protein kinase C (PKC) activity, suggesting that PKC may act directly on the intracellular source of Zn(2+). We identified a conserved PKC phosphorylation site at serine-32 (S32) of metallothionein (MT) that was important in modulating Zn(2+)-regulated gene expression and conferring excitotoxic tolerance. Importantly, we observed increased PKC-induced serine phosphorylation in immunopurified MT1, but not in mutant MT1(S32A). These results indicate that neuronal Zn(2+) serves as an important, highly regulated signaling component responsible for the initiation of a neuroprotective pathway.
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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.