ArticleMolecular neurobiology2012
Glutathione S-transferase pi mediates MPTP-induced c-Jun N-terminal kinase activation in the nigrostriatal pathway.
Article in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Transcriptome profiling of neurexin- and neuroligin-deficient Caenorhabditis elegans reveals pathways underlying developmental and behavioral dysfunction.Research square · 2026Article
- Low dose ionising radiation elicits MPTP comparable alterations in locomotor Function, oxidative balance and mitochondrial homeostasis in zebrafish embryos.Scientific reports · 2025Article
- Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers.Antioxidants (Basel, Switzerland) · 2024Review
- Overexpression of Glutathione S-Transferases in Human Diseases: Drug Targets and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2023Review
- Modulation of redox homeostasis: A strategy to overcome cancer drug resistance.Frontiers in pharmacology · 2023Review
- Icariin Induces Triple-Negative Breast Cancer Cell Apoptosis and Suppresses Invasion by Inhibiting the JNK/c-Jun Signaling Pathway.Drug design, development and therapy · 2023Article
- ROS/JNK/C-Jun Pathway is Involved in Chaetocin Induced Colorectal Cancer Cells Apoptosis and Macrophage Phagocytosis Enhancement.Frontiers in pharmacology · 2021Article
- Role of RONS and eIFs in Cancer Progression.Oxidative medicine and cellular longevity · 2021Review
- The Influence of Reactive Oxygen Species in the Immune System and Pathogenesis of Multiple Sclerosis.Autoimmune diseases · 2020Review
- Inhibition of glutathione S-transferase-pi triggers c-jun N-terminal kinase-dependent neuronal death in Zn-induced Parkinsonism.Molecular and cellular biochemistry · 2019Article
- Glutathione transferases: substrates, inihibitors and pro-drugs in cancer and neurodegenerative diseases.Oncogenesis · 2018Review
- Cellular Stresses and Stress Responses in the Pathogenesis of Insulin Resistance.Oxidative medicine and cellular longevity · 2018Review
- The Dietary Components Carnosic Acid and Carnosol as Neuroprotective Agents: a Mechanistic View.Molecular neurobiology · 2016Review
- Neuroprotective Effects of β-Asarone Against 6-Hydroxy Dopamine-Induced Parkinsonism via JNK/Bcl-2/Beclin-1 Pathway.Molecular neurobiology · 2016Article
- ROS and ROS-Mediated Cellular Signaling.Oxidative medicine and cellular longevity · 2016Review
- Altered protein S-glutathionylation identifies a potential mechanism of resistance to acetaminophen-induced hepatotoxicity.The Journal of pharmacology and experimental therapeutics · 2015Article
- Glutathione metabolism and Parkinson's disease.Free radical biology & medicine · 2013Review
- Ubiquitin-proteasome system impairment and MPTP-induced oxidative stress in the brain of C57BL/6 wild-type and GSTP knockout mice.Molecular neurobiology · 2013Article
- Article
- Tauroursodeoxycholic acid prevents MPTP-induced dopaminergic cell death in a mouse model of Parkinson's disease.Molecular neurobiology · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is a progressive movement disorder resulting from the death of dopaminergic neurons in the substantia nigra. Neurotoxin-based models of PD using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) recapitulate the neurological features of the disease, triggering a cascade of deleterious events through the activation of the c-Jun N-terminal kinase (JNK). The molecular mechanisms underlying the regulation of JNK activity under cellular stress conditions involve the activation of several upstream kinases along with the fine-tuning of different endogenous JNK repressors. Glutathione S-transferase pi (GSTP), a phase II detoxifying enzyme, has been shown to inhibit JNK-activated signaling by protein-protein interactions, preventing c-Jun phosphorylation and the subsequent trigger of the cell death cascade. Here, we use C57BL/6 wild-type and GSTP knockout mice treated with MPTP to evaluate the regulation of JNK signaling by GSTP in both the substantia nigra and the striatum. The results presented herein show that GSTP knockout mice are more susceptible to the neurotoxic effects of MPTP than their wild-type counterparts. Indeed, the administration of MPTP induces a progressive demise of nigral dopaminergic neurons together with the degeneration of striatal fibers at an earlier time-point in the GSTP knockout mice when compared to the wild-type mice. Also, MPTP treatment leads to increased p-JNK levels and JNK catalytic activity in both wild-type and GSTP knockout mice midbrain and striatum. Moreover, our results demonstrate that in vivo GSTP acts as an endogenous regulator of the MPTP-induced cellular stress response by controlling JNK activity through protein-protein interactions.
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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.