ArticleThe Biochemical journal2014
Impaired selenoprotein expression in brain triggers striatal neuronal loss leading to co-ordination defects in mice.
Article in The Biochemical journal, 2014. 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, 52 citations in OpenAlex.
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Iron and selenium: At the crossroads of development and death in oligodendrocytes.Archives of biochemistry and biophysics · 2025Review
- Severe neurodevelopmental phenotype, diagnostic, and treatment challenges in patients with SECISBP2 deficiency.Genetics in medicine : official journal of the American College of Medical Genetics · 2024Article
- Selenoprotein I (selenoi) as a critical enzyme in the central nervous system.Archives of biochemistry and biophysics · 2022Article
- High-Resolution Ribosome Profiling Reveals Gene-Specific Details of UGA Re-Coding in Selenoprotein Biosynthesis.Biomolecules · 2022Article
- Observational
- Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto's Thyroiditis.International journal of molecular sciences · 2021Article
- Cell-penetrating, antioxidant SELENOT mimetic protects dopaminergic neurons and ameliorates motor dysfunction in Parkinson's disease animal models.Redox biology · 2021Article
- Serum Selenium Status as a Diagnostic Marker for the Prognosis of Liver Transplantation.Nutrients · 2021Article
- The Neurobiology of Selenium: Looking Back and to the Future.Frontiers in neuroscience · 2021Review
- Rutin and Selenium Co-administration Reverse 3-Nitropropionic Acid-Induced Neurochemical and Molecular Impairments in a Mouse Model of Huntington's Disease.Neurotoxicity research · 2020Article
- Ribosome profiling of selenoproteinsThe Journal of biological chemistry · 2019Article
- Thyroid Hormone Hyposensitivity: From Genotype to Phenotype and Back.Frontiers in endocrinology · 2019Review
- Selenocysteine tRNAMethods in molecular biology (Clifton, N.J.) · 2018Article
- A selenium species in cerebrospinal fluid predicts conversion to Alzheimer's dementia in persons with mild cognitive impairment.Alzheimer's research & therapy · 2017Article
- Thyroid Hormone Metabolism Defects in a Mouse Model of SBP2 Deficiency.Endocrinology · 2017Article
- Rapid polygenic response to secondary contact in a hybrid species.Proceedings. Biological sciences · 2017Article
- Human selenoprotein P and S variant mRNAs with different numbers of SECIS elements and inferences from mutant mice of the roles of multiple SECIS elements.Open biology · 2016Article
- Selenoprotein T Exerts an Essential Oxidoreductase Activity That Protects Dopaminergic Neurons in Mouse Models of Parkinson's Disease.Antioxidants & redox signaling · 2016Article
- Paradoxical Roles of Antioxidant Enzymes: Basic Mechanisms and Health Implications.Physiological reviews · 2016Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Secisbp2 [SECIS (selenocysteine insertion sequence)-binding protein 2] binds to SECIS elements located in the 3'-UTR region of eukaryotic selenoprotein mRNAs. It facilitates the incorporation of the rare amino acid selenocysteine in response to UGA codons. Inactivation of Secisbp2 in hepatocytes greatly reduced selenoprotein levels. Neuron-specific inactivation of Secisbp2 (CamK-Cre; Secisbp2fl/fl) reduced cerebral expression of selenoproteins to a lesser extent than inactivation of tRNA[Ser]Sec. This allowed us to study the development of cortical PV (parvalbumin)+ interneurons, which are completely lost in tRNA[Ser]Sec mutants. PV+ interneuron density was reduced in the somatosensory cortex, hippocampus and striatum. In situ hybridization for Gad67 (glutamic acid decarboxylase 67) confirmed the reduction of GABAergic (where GABA is γ-aminobutyric acid) interneurons. Because of the obvious movement phenotype involving a broad dystonic gait, we suspected basal ganglia dysfunction. Tyrosine hydroxylase expression was normal in substantia nigra neurons and their striatal terminals. However the densities of striatal PV+ and Gad67+ neurons were decreased by 65% and 49% respectively. Likewise, the density of striatal cholinergic neurons was reduced by 68%. Our observations demonstrate that several classes of striatal interneurons depend on selenoprotein expression. These findings may offer an explanation for the movement phenotype of selenoprotein P-deficient mice and the movement disorder and mental retardation described in a patient carrying SECISBP2 mutations.
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