ArticleHuman molecular genetics2008
Sodium-potassium ATPase 1 subunit is a molecular partner of Wolframin, an endoplasmic reticulum protein involved in ER stress.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- WFS1 autosomal dominant variants linked with hearing loss: update on structural analysis and cochlear implant outcome.BMC medical genomics · 2023Pooled it
- WFS1 Deficiency Impairs PIAS4-Associated SUMOylation and Increases Ubiquitin-Mediated Spermatogenesis-Related Protein Degradation Leading to Testicular Male Infertility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Synaptic Alterations Are Preceding the Axonal Loss in Optic Atrophy of Wolfram Syndrome Mouse Model.bioRxiv : the preprint server for biology · 2026Article
- Synaptic alterations are preceding the axonal loss in optic atrophy of Wolfram syndrome mouse model.Frontiers in neuroscience · 2026Article
- Do wolframin, P-glycoprotein, and GRP78/BiP cooperate to alter the response of L1210 cells to endoplasmic reticulum stress or drug sensitivity?Cancer cell international · 2025Article
- Topology ofPediatric diabetes · 2025Article
- Clinical Characteristics and Audiological Profiles of Patients with Pathogenic Variants ofJournal of clinical medicine · 2024Article
- Review
- Wolfram Syndrome Type I Case Report and Review-Focus on Early Diagnosis and Genetic Variants.Medicina (Kaunas, Lithuania) · 2024Review
- Ataxia and Hypogonadism: a Review of the Associated Genes and Syndromes.Cerebellum (London, England) · 2024Review
- Comprehensive overview of disease models for Wolfram syndrome: toward effective treatments.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Review
- Genomics of Wolfram Syndrome 1 (WFS1).Biomolecules · 2023Review
- GLP-1R agonists demonstrate potential to treat Wolfram syndrome in human preclinical models.Diabetologia · 2023Article
- Wfs1Cell death & disease · 2023Article
- Depletion of WFS1 compromises mitochondrial function in hiPSC-derived neuronal models of Wolfram syndrome.Stem cell reports · 2023Article
- Mutation analysis of pathogenic non-synonymous single nucleotide polymorphisms (nsSNPs) in WFS1 gene through computational approaches.Scientific reports · 2023Article
- Article
- Complex clinical manifestations and new insights in RNA sequencing of children with diabetes andFrontiers in endocrinology · 2023Article
- Mutation analysis of the WFS1 gene in a Chinese family with autosomal-dominant non-syndrome deafness.Scientific reports · 2022Article
- Wolframin deficiency is accompanied with metabolic inflexibility in rat striated muscles.Biochemistry and biophysics reports · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Wolfram syndrome, an autosomal recessive disorder characterized by diabetes mellitus and optic atrophy, is caused by mutations in the WFS1 gene encoding an endoplasmic reticulum (ER) membrane protein, Wolframin. Although its precise functions are unknown, Wolframin deficiency increases ER stress, impairs cell cycle progression and affects calcium homeostasis. To gain further insight into its function and identify molecular partners, we used the WFS1-C-terminal domain as bait in a yeast two-hybrid screen with a human brain cDNA library. Na+/K+ ATPase beta1 subunit was identified as an interacting clone. We mapped the interaction to the WFS1 C-terminal and transmembrane domains, but not the N-terminal domain. Our mapping data suggest that the interaction most likely occurs in the ER. We confirmed the interaction by co-immunoprecipitation in mammalian cells and with endogenous proteins in JEG3 placental cells, neuroblastoma SKNAS and pancreatic MIN6 beta cells. Na+/K+ ATPase beta1 subunit expression was reduced in plasma membrane fractions of human WFS1 mutant fibroblasts and WFS1 knockdown MIN6 pancreatic beta-cells compared with wild-type cells; Na+/K+ ATPase alpha1 subunit expression was also reduced in WFS-depleted MIN6 beta cells. Induction of ER stress in wild-type cells only partly accounted for the reduced Na+/K+ ATPase beta1 subunit expression observed. We conclude that the interaction may be important for Na+/K+ ATPase beta1 subunit maturation; loss of this interaction may contribute to the pathology seen in Wolfram syndrome via reductions in sodium pump alpha1 and beta1 subunit expression in pancreatic beta-cells.
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