ArticleProceedings of the National Academy of Sciences of the United States of America2018
Golgi stress response reprograms cysteine metabolism to confer cytoprotection in Huntington's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 123 citations in OpenAlex.
- Multifaceted roles for persulfide species in redox chemical biology.Nature chemical biology · 2026Review
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- Decreased Plasma Concentration of Hydrogen Sulfide in Hospitalized COVID-19 Patients: A Novel Determinant of Mortality?Antioxidants (Basel, Switzerland) · 2026Article
- Hydrogen Sulfide Signaling in Neurodegenerative Movement Disorders.Handbook of experimental pharmacology · 2026Review
- Cystathionine γ-lyase is a major regulator of cognitive function through neurotrophin signaling and neurogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- Profiling the landscape of cysteine posttranslational modifications in brain aging and neurodegeneration.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Gasotransmitter signaling in the brain: New frontiers for therapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Intersection of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Hydrogen sulfide/polysulfides signaling and neuronal diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Small-molecule probes for imaging and impairing the Golgi apparatus in cancer.RSC medicinal chemistry · 2025Review
- The Supersulfide-Producing Activity of Rat Cystathionine γ-Lyase Is Irreversibly Inactivated by L-CysNO but Not by L-GSNO.Antioxidants (Basel, Switzerland) · 2025Article
- Diabetes mellitus and the key role of endoplasmic reticulum stress in pancreatic β cells.Nature reviews. Endocrinology · 2025Review
- Sequential Targeting Chondroitin Sulfate-Bilirubin Nanomedicine Attenuates Osteoarthritis via Reprogramming Lipid Metabolism in M1 Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Natural sulfur compounds in mental health and neurological disorders: insights from observational and intervention studies.Frontiers in nutrition · 2025Review
- Cerebral endothelial 3-mercaptopyruvate sulfurtransferase improves ischemia-induced cognitive impairmentActa pharmaceutica Sinica. B · 2025Article
- Dietary methionine supplementation improves cognitive dysfunction associated with transsulfuration pathway upregulation in subacute aging mice.NPJ science of food · 2024Article
- Giantin mediates Golgi localization of Gal3-O-sulfotransferases and affects salivary mucin sulfation in patients with Sjögren's disease.JCI insight · 2024Article
- HScience advances · 2024Article
- Golgiphagy: a novel selective autophagy to the fore.Cell & bioscience · 2024Review
7 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Golgi stress response is emerging as a physiologic process of comparable importance to endoplasmic reticulum (ER) and mitochondrial stress responses. However, unlike ER stress, the identity of the signal transduction pathway involved in the Golgi stress response has been elusive. We show that the Golgi stressor monensin acts via the PKR-like ER kinase/Activating Transcription Factor 4 pathway. ATF4 is the master regulator of amino acid metabolism, which is induced during amino acid depletion and other forms of stress. One of the genes regulated by ATF4 is the biosynthetic enzyme for cysteine, cystathionine γ-lyase (CSE), which also plays central roles in maintenance of redox homeostasis. Huntington's disease (HD), a neurodegenerative disorder, is associated with disrupted cysteine metabolism caused by depletion of CSE leading to abnormal redox balance and stress response. Thus, restoring CSE function and cysteine disposition may be beneficial in HD. Accordingly, we harnessed the monensin-ATF4-signaling cascade to stimulate CSE expression by preconditioning cells with monensin, which restores cysteine metabolism and an optimal stress response in HD. These findings have implications for treatment of HD and other diseases associated with redox imbalance and dysregulated ATF4 signaling.
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