ArticleMolecular and cellular biology2008
Increased insulin action in SKIP heterozygous knockout mice.
Article in Molecular and cellular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- The power of five - inositol polyphosphate 5-phosphatase gene mutations at the intersection of development and disease.FEBS letters · 2026Review
- Crystal structure of human INPP5K with an allosteric inhibitor reveals the structural basis for species specific potency.Scientific reports · 2026Article
- Modulating PAK1: Accessory Proteins as Promising Therapeutic Targets.Biomolecules · 2025Review
- Knockdown of INPP5K compromises the differentiation of N2A cells.Frontiers in molecular neuroscience · 2024Article
- Phosphoinositides in New Spaces.Cold Spring Harbor perspectives in biology · 2023Review
- Increased body mass index is linked to systemic inflammation through altered chromatin co-accessibility in human preadipocytes.Nature communications · 2023Article
- PI(4,5)PScience advances · 2023Article
- INPP5K and Atlastin-1 maintain the nonuniform distribution of ER-plasma membrane contacts in neurons.Life science alliance · 2021Article
- Defective lysosome reformation during autophagy causes skeletal muscle disease.The Journal of clinical investigation · 2021Article
- Induced Dimerization Tools to Deplete Specific Phosphatidylinositol Phosphates.Methods in molecular biology (Clifton, N.J.) · 2021Article
- PTEN and Other PtdIns(3,4,5)PInternational journal of molecular sciences · 2020Review
- Phosphoinositide lipids in primary cilia biology.The Biochemical journal · 2020Review
- PI(3,4)P2 Signaling in Cancer and Metabolism.Frontiers in oncology · 2020Review
- The Prediction and Prognostic Significance of INPP5K Expression in Patients with Liver Cancer.BioMed research international · 2020Article
- A Recurrent Pathogenic Variant ofFrontiers in genetics · 2020Article
- The inositol 5-phosphatase INPP5K participates in the fine control of ER organization.The Journal of cell biology · 2018Article
- Mutations in INPP5K, Encoding a Phosphoinositide 5-Phosphatase, Cause Congenital Muscular Dystrophy with Cataracts and Mild Cognitive Impairment.American journal of human genetics · 2017Article
- Phosphatidylinositolphosphate phosphatase activities and cancer.Journal of lipid research · 2016Review
- Lowered Expression of Tumor Suppressor Candidate MYO1C Stimulates Cell Proliferation, Suppresses Cell Adhesion and Activates AKT.PloS one · 2016Article
- Phosphatidylinositol 3,4,5-Trisphosphate Phosphatase SKIP Links Endoplasmic Reticulum Stress in Skeletal Muscle to Insulin Resistance.Molecular and cellular biology · 2016Article
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Insulin controls glucose homeostasis and lipid metabolism, and insulin impairment plays a critical role in the pathogenesis of diabetes mellitus. Human skeletal muscle and kidney enriched inositol polyphosphate phosphatase (SKIP) is a member of the phosphatidylinositol 3,4,5-trisphosphate phosphatase family (T. Ijuin et al. J. Biol. Chem. 275:10870-10875, 2000; T. Ijuin and T. Takenawa, Mol. Cell. Biol. 23:1209-1220, 2003). Previous studies showed that SKIP negatively regulates insulin-induced phosphatidylinositol 3-kinase signaling (Ijuin and Takenawa, Mol. Cell. Biol. 23:1209-1220, 2003). We now have generated mice with a targeted mutation of the mouse ortholog of the human SKIP gene, Pps. Adult heterozygous Pps mutant mice show increased insulin sensitivity and reduced diet-induced obesity with increased Akt/protein kinase B (PKB) phosphorylation in skeletal muscle but not in adipose tissue. The insulin-induced uptake of 2-deoxyglucose into the isolated soleus muscle was significantly enhanced in Pps mutant mice. A hyperinsulinemic-euglycemic clamp study also revealed a significant increase in the rate of systemic glucose disposal in Pps mutant mice without any abnormalities in hepatic glucose production. Furthermore, in vitro knockdown studies in L6 myoblast cells revealed that reduction of SKIP expression level increased insulin-stimulated Akt/PKB phosphorylation and 2-deoxyglucose uptake. These results imply that SKIP regulates insulin signaling in skeletal muscle. Thus, SKIP may be a promising pharmacologic target for the treatment of insulin resistance and diabetes.
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Registered trials
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