ArticleJournal of molecular neuroscience : MN2013
Upregulation of sestrin-2 expression via P53 protects against 1-methyl-4-phenylpyridinium (MPP+) neurotoxicity.
Article in Journal of molecular neuroscience : MN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 45 citations in OpenAlex.
- Interplay Between Sestrin Proteins and Ferroptosis: A Comprehensive Review of Regulatory Mechanisms.Molecular biotechnology · 2026Review
- Review
- Sestrins: a new therapeutic target for endothelial dysfunction and cardiovascular disease prevention.Annals of medicine · 2025Review
- Sestrin2 can alleviate endoplasmic reticulum stress to improve traumatic brain injury by activating AMPK/mTORC1 signaling pathway.Metabolic brain disease · 2024Review
- The effects of whole-body vibration therapy on immune and brain functioning: current insights in the underlying cellular and molecular mechanisms.Frontiers in neurology · 2024Review
- Targeting the p53 signaling pathway in cancers: Molecular mechanisms and clinical studies.MedComm · 2023Review
- Sestrin2 as a Protective Shield against Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Melatonin Ameliorates Ovarian Hyperstimulation Syndrome (OHSS) through SESN2 Regulated Antiapoptosis.Obstetrics and gynecology international · 2023Article
- Oxidative Stress-Induced Protein of SESTRIN2 in Cardioprotection Effect.Disease markers · 2022Review
- Potential Roles of Sestrin2 in Alzheimer's Disease: Antioxidation, Autophagy Promotion, and Beyond.Biomedicines · 2021Review
- Target Sestrin2 to Rescue the Damaged Organ: Mechanistic Insight into Its Function.Oxidative medicine and cellular longevity · 2021Review
- Molecular crosstalk between cancer and neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2020Review
- Functional Role of p53 in the Regulation of Chemical-Induced Oxidative Stress.Oxidative medicine and cellular longevity · 2020Review
- Upregulated expression of the antioxidant sestrin 2 identified by transcriptomic analysis of Japanese encephalitis virus-infected SH-SY5Y neuroblastoma cells.Virus genes · 2019Article
- Emerging Roles of Sestrins in Neurodegenerative Diseases: Counteracting Oxidative Stress and Beyond.Journal of clinical medicine · 2019Review
- Discovery of NV-5138, the first selective Brain mTORC1 activator.Scientific reports · 2019Article
- Sestrin2: Its Potential Role and Regulatory Mechanism in Host Immune Response in Diseases.Frontiers in immunology · 2019Review
- Sestrins at the Interface of ROS Control and Autophagy Regulation in Health and Disease.Oxidative medicine and cellular longevity · 2019Review
- RBX1-mediated ubiquitination of SESN2 promotes cell death upon prolonged mitochondrial damage in SH-SY5Y neuroblastoma cells.Molecular and cellular biochemistry · 2018Article
- SESN2 facilitates mitophagy by helping Parkin translocation through ULK1 mediated Beclin1 phosphorylation.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sestrin-2 (SESN2) is a conserved antioxidant protein that is activated upon oxidative stress and protects cells against reactive oxygen species (ROS). However, the role of SESN2 in neurodegenerative diseases, especially in Parkinson's disease (PD), has not yet been elucidated. In this study, we found that expression of SESN2 is elevated in the midbrain of patients with PD. Moreover, in vitro experiments display that the drug 1-methyl-4-phenylpyridinium (MPP+) induces the expression of SESN2 in SH-SY5Y cells in a time- and dose-dependent manner. Our results show that p53 is activated by MPP+. Importantly, inhibition of p53 using small RNA interferences abolishes the increased SESN2 levels induced by MPP+, suggesting that the inductive effect of MPP+ on SESN2 is mediated by p53. Furthermore, knockdown of SESN2 using small RNA interferences promotes MPP+-related neurotoxicity by attenuating oxidative stress, mitochondrial dysfunction, and apoptosis. All these data imply that the induction of SESN2 produces a protective effect in PD.
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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.