ArticleGlia2013
Glutamate dehydrogenase 1 and SIRT4 regulate glial development.
Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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.
The trial behind it
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- SIRT4 Alleviates Retinal Ischemia-Reperfusion Injury Via Mediating Astrocytes Lipid Metabolism and Mitochondrial Function.Investigative ophthalmology & visual science · 2026Article
- Review
- The role of glutamate dehydrogenase in the ageing brain.Frontiers in pharmacology · 2025Review
- Alleviating Neurodegenerative Diseases Associated with Mitochondrial Defects by Therapeutic Biomolecules.Current topics in medicinal chemistry · 2024Review
- Targeting Mitochondrial Sirtuins in Age-Related Neurodegenerative Diseases and Fibrosis.Aging and disease · 2023Review
- Advances of SIRT4 in cancer metabolism and therapy.Pediatric discovery · 2023Review
- Sirtuins: Promising Therapeutic Targets to Treat Ischemic Stroke.Biomolecules · 2023Review
- Amino acids downregulate SIRT4 to detoxify ammonia through the urea cycle.Nature metabolism · 2023Article
- Glutamate dehydrogenase hyperinsulinism: mechanisms, diagnosis, and treatment.Orphanet journal of rare diseases · 2023Review
- Exploring the Multi-Faceted Role of Sirtuins in Glioblastoma Pathogenesis and Targeting Options.International journal of molecular sciences · 2022Review
- Roles of sirtuin family members in chronic obstructive pulmonary disease.Respiratory research · 2022Review
- Features Neurohumoral and Immune Profile in Children with Functional Disorders of the Autonomic Nervous System Associated with Sirtuin Gene SIRT1 (rs7069102) Polymorphism.Bulletin of experimental biology and medicine · 2022Article
- Paeoniflorin Enhances the Sensitivity of ER-Positive Breast Cancer Cells to Tamoxifen through Promoting Sirtuin 4.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Proteomic profiling reveals the potential mechanisms and regulatory targets of sirtuin 4 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's mouse model.Frontiers in neuroscience · 2022Article
- SIRT4 Is Highly Expressed in Retinal Müller Glial Cells.Frontiers in neuroscience · 2022Article
- Functions of mammalian SIRT4 in cellular metabolism and research progress in human cancer.Oncology letters · 2020Review
- Anabolic SIRT4 Exerts Retrograde Control over TORC1 Signaling by Glutamine Sparing in the Mitochondria.Molecular and cellular biology · 2020Article
- Research Progress of Sirtuin4 in Cancer.Frontiers in oncology · 2020Review
- Recovery of Olfactory Function After Excitotoxic Lesion of the Olfactory Bulbs Is Associated with Increases in Bulbar SIRT1 and SIRT4 Expressions.Molecular neurobiology · 2019Article
- Mitochondrial Function, Metabolic Regulation, and Human Disease Viewed through the Prism of Sirtuin 4 (SIRT4) Functions.Journal of proteome research · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Congenital hyperinsulinism/hyperammonemia (HI/HA) syndrome is caused by an activation mutation of glutamate dehydrogenase 1 (GDH1), a mitochondrial enzyme responsible for the reversible interconversion between glutamate and α-ketoglutarate. The syndrome presents clinically with hyperammonemia, significant episodic hypoglycemia, seizures, and frequent incidences of developmental and learning defects. Clinical research has implicated that although some of the developmental and neurological defects may be attributed to hypoglycemia, some characteristics cannot be ascribed to low glucose and as hyperammonemia is generally mild and asymptomatic, there exists the possibility that altered GDH1 activity within the brain leads to some clinical changes. GDH1 is allosterically regulated by many factors, and has been shown to be inhibited by the ADP-ribosyltransferase sirtuin 4 (SIRT4), a mitochondrially localized sirtuin. Here we show that SIRT4 is localized to mitochondria within the brain. SIRT4 is highly expressed in glial cells, specifically astrocytes, in the postnatal brain and in radial glia during embryogenesis. Furthermore, SIRT4 protein decreases in expression during development. We show that factors known to allosterically regulate GDH1 alter gliogenesis in CTX8 cells, a novel radial glial cell line. We find that SIRT4 and GDH1 overexpression play antagonistic roles in regulating gliogenesis and that a mutant variant of GDH1 found in HI/HA patients accelerates the development of glia from cultured radial glia cells.
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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.