ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2020
Prohibitin S-Nitrosylation Is Required for the Neuroprotective Effect of Nitric Oxide in Neuronal Cultures.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Oxidative Metabolism in Brain Ischemia and Preconditioning: Two Sides of the Same Coin.Antioxidants (Basel, Switzerland) · 2024Review
- Molecular Mechanisms of Neuroprotection after the Intermittent Exposures of Hypercapnic Hypoxia.International journal of molecular sciences · 2024Review
- S-Glutathionylation and S-Nitrosylation in Mitochondria: Focus on Homeostasis and Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- The function of prohibitins in mitochondria and the clinical potentials.Cancer cell international · 2022Review
- Nitrosative stress in Parkinson's disease.NPJ Parkinson's disease · 2022Review
- Prohibitins in neurodegeneration and mitochondrial homeostasis.Frontiers in aging · 2022Review
- Prohibitins: A Key Link between Mitochondria and Nervous System Diseases.Oxidative medicine and cellular longevity · 2022Review
- Role of Nitric Oxide and Protein S-Nitrosylation in Ischemia-Reperfusion Injury.Antioxidants (Basel, Switzerland) · 2021Review
- Role of Prohibitins in Aging and Therapeutic Potential Against Age-Related Diseases.Frontiers in genetics · 2021Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Prohibitin (PHB) is a critical protein involved in many cellular activities. In brain, PHB resides in mitochondria, where it forms a large protein complex with PHB2 in the inner TFmembrane, which serves as a scaffolding platform for proteins involved in mitochondrial structural and functional integrity. PHB overexpression at moderate levels provides neuroprotection in experimental brain injury models. In addition, PHB expression is involved in ischemic preconditioning, as its expression is enhanced in preconditioning paradigms. However, the mechanisms of PHB functional regulation are still unknown. Observations that nitric oxide (NO) plays a key role in ischemia preconditioning compelled us to postulate that the neuroprotective effect of PHB could be regulated by NO. Here, we test this hypothesis in a neuronal model of ischemia-reperfusion injury and show that NO and PHB are mutually required for neuronal resilience against oxygen and glucose deprivation stress. Further, we demonstrate that NO post-translationally modifies PHB through protein S-nitrosylation and regulates PHB neuroprotective function, in a nitric oxide synthase-dependent manner. These results uncover the mechanisms of a previously unrecognized form of molecular regulation of PHB that underlies its neuroprotective function.
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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.