ArticleGene therapy2016
Overexpression of a glucokinase point mutant in the treatment of diabetes mellitus.
Article in Gene therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Role of the xenobiotic-activated pregnane X receptor in type 1 and type 2 diabetes in male mice.Biochemical pharmacology · 2026Article
- Cell Therapies and Gene Therapy for Diabetes: Current Progress.Current diabetes reviews · 2025Review
- Evaluation of the anti-diabetic and anti-inflammatory potentials of curcumin nanoparticle in diabetic rat induced by streptozotocin.Open veterinary journal · 2024Article
- Genetic and Pharmacological Inhibition of GCN2 Ameliorates Hyperglycemia and Insulin Resistance in Type 2 Diabetic Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Citrullination of glucokinase is linked to autoimmune diabetes.Nature communications · 2022Article
- Biomarkers of autoimmunity and beta cell metabolism in type 1 diabetes.Frontiers in immunology · 2022Review
- Comprehensive analysis of liver and blood miRNA in precancerous conditions.Scientific reports · 2020Article
- SNPs in the 3'-untranslated region ofJournal of diabetes and metabolic disorders · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucokinase (GCK) is an important enzyme critical for glucose metabolism, and has been targeted as such in the pursuit of a cure for diabetes mellitus. We show that streptozotocin (STZ)-induced diabetic murine model exhibits low GCK expression with high blood glucose levels; moreover, aggravated glomerulonephritis is observed in the model when there is IL10 deficiency. Although T cells infiltrate into the liver and pancreas in STZ-induced diabetes mice, T helper 1 (Th1) and T helper 17 (Th17) cells decrease significantly with STZ addition in in vitro polarization. Using a mutant GCK gene (GCK 262) with a knocked out cytosine at position 2643 results in lower protein expression and more ubiquitination-led protein degradation compared with wild-type GCK (GCK 261). We further observed that hsa-mir-1302 can bind to 3'-untranslated region of mutant GCK, which can decrease GCK mRNA translation. Finally, delivery of mutant GCK by subcutaneous injection is more effective at decreasing blood glucose in the STZ-treated (STZ) murine diabetes model than insulin treatment alone. Similarly, mutant GCK consistently and moderately decreases blood glucose levels in GK rats over a period of 12 and 70 days without inducing hypoglycemia, whereas insulin is only effective over 12 h. These results suggest that mutant GCK may be a future cure for diabetes.
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