ArticleScientific reports2023
Skeletal muscle overexpression of sAnk1.5 in transgenic mice does not predispose to type 2 diabetes.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 4 citations in OpenAlex.
- GWAS-by-subtraction reveals new genetic architecture and health implications of type 2 diabetes-independent gestational diabetes mellitus.Genome medicine · 2026Article
- Genome writing and Targeted Delivery of thebioRxiv : the preprint server for biology · 2026Article
- Ankyrin-B modulates mitochondrial fission in skeletal muscle and is required for optimal endurance exercise capacity.Nature communications · 2025Article
- Analysis of the SARS-CoV-2 inactivation mechanism using violet-blue light (405 nm).Applied and environmental microbiology · 2025Article
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Authors and funding
13 authors at 4 institutions in 4 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Genome-wide association studies (GWAS) and cis-expression quantitative trait locus (cis-eQTL) analyses indicated an association of the rs508419 single nucleotide polymorphism (SNP) with type 2 diabetes (T2D). rs508419 is localized in the muscle-specific internal promoter (P2) of the ANK1 gene, which drives the expression of the sAnk1.5 isoform. Functional studies showed that the rs508419 C/C variant results in increased transcriptional activity of the P2 promoter, leading to higher levels of sAnk1.5 mRNA and protein in skeletal muscle biopsies of individuals carrying the C/C genotype. To investigate whether sAnk1.5 overexpression in skeletal muscle might predispose to T2D development, we generated transgenic mice (Tg
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