ArticleDiabetologia2017
The MST3/STK24 kinase mediates impaired fasting blood glucose after a high-fat diet.
Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting STE20-type kinase MST3 improves metabolic dysfunction-associated steatohepatitis without affecting hepatocellular carcinoma development in mice.BMC medicine · 2026Article
- Inhibition of GCKIII kinases STK25 and MST3 mitigates organ lipotoxicity and enhances metabolic resilience under nutritional stress.BMC medicine · 2025Article
- MST3 Regulates AMPK and YAP-Hippo Signaling in Cell Models Relevant to Renal Fibrosis.Biomolecules & therapeutics · 2025Article
- GCKIII kinases control hepatocellular lipid homeostasis via shared mode of action.Journal of lipid research · 2024Article
- Genetic Ablation of STE20-Type Kinase MST4 Does Not Alleviate Diet-Induced MASLD Susceptibility in Mice.International journal of molecular sciences · 2024Article
- Epinephrine inhibits PI3Kα via the Hippo kinases.Cell reports · 2023Article
- Review
- Molecular mechanisms involved in regulating protein activity and biological function of MST3.Cell division · 2023Review
- NDR kinase tricornered genetically interacts with Ccm3 and metabolic enzymes in Drosophila melanogaster tracheal development.G3 (Bethesda, Md.) · 2023Article
- Article
- The oncogenic role of MST3 in human gastric cancer.American journal of cancer research · 2018Article
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Authors and funding
12 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe identification of mediators in the pathogenesis of type 2 diabetes mellitus is essential for the full understanding of this disease. Protein kinases are especially important because of their potential as pharmacological targets. The goal of this study was to investigate whether mammalian sterile-20 3 (MST3/STK24), a stress-regulated kinase, is involved in metabolic alterations in obesity.
methodsGlucose regulation of Mst3 (also known as Stk24)-knockout mice was analysed both in 129;C57 mixed background mice and in C57/BL6J mice fed normally or with a high-fat diet (HFD). This work was complemented with an analysis of the insulin signalling pathway in cultured human liver cells made deficient in MST3 using RNA interference.
resultsMST3 is phosphorylated in the livers of mice subject to an obesity-promoting HFD, and its deficiency lowers the hyperglycaemia, hyperinsulinaemia and insulin resistance that the animals develop with this diet, an effect that is seen even without complete inactivation of the kinase. Lack of MST3 results in activation of the insulin signalling pathway downstream of IRS1, in both cultured liver cells and the liver of animals after HFD. This effect increases the inhibition of forkhead box (FOX)O1, with subsequent downregulation of the expression of gluconeogenic enzymes. CONCLUSIONS/
interpretationMST3 inhibits the insulin signalling pathway and is important in the development of insulin resistance and impaired blood glucose levels after an HFD.
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