ArticleDiabetologia2005
Protein kinase-zeta interacts with munc18c: role in GLUT4 trafficking.
Article in Diabetologia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 47 citations in OpenAlex.
- Combined Hyperglycemia- and Hyperinsulinemia-Induced Insulin Resistance in Adipocytes Is Associated With Dual Signaling Defects Mediated by PKC-ζ.Endocrinology · 2018Article
- Disruption of protein complexes containing protein phosphatase 2B and Munc18c reduces the secretion of von Willebrand factor from endothelial cells.Journal of thrombosis and haemostasis : JTH · 2017Article
- Unacylated ghrelin restores insulin and autophagic signaling in skeletal muscle of diabetic mice.Pflugers Archiv : European journal of physiology · 2015Article
- Mathematical modeling of the insulin signal transduction pathway for prediction of insulin sensitivity from expression data.Molecular genetics and metabolism · 2015Article
- Abi3bp is a multifunctional autocrine/paracrine factor that regulates mesenchymal stem cell biology.Stem cells (Dayton, Ohio) · 2013Article
- Cardiac PI3K-Akt impairs insulin-stimulated glucose uptake independent of mTORC1 and GLUT4 translocation.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Sequestosome 1/p62, a scaffolding protein, is a newly identified partner of IRS-1 protein.The Journal of biological chemistry · 2012Article
- Protein expression of PKCZ (Protein Kinase C Zeta), Munc18c, and Syntaxin-4 in the insulin pathway in endometria of patients with polycystic ovary syndrome (PCOS).Reproductive biology and endocrinology : RB&E · 2012Article
- Effects of exercise on AMPK signaling and downstream components to PI3K in rat with type 2 diabetes.PloS one · 2012Article
- Signaling, cytoskeletal and membrane mechanisms regulating GLUT4 exocytosis.Trends in endocrinology and metabolism: TEM · 2011Review
- Protein phosphatase 2B inhibition promotes the secretion of von Willebrand factor from endothelial cells.Journal of thrombosis and haemostasis : JTH · 2009Article
- Activation of atypical protein kinase Czeta toward TC10 is regulated by high-fat diet and aerobic exercise in skeletal muscle.Metabolism: clinical and experimental · 2008Article
- Substrate uptake and metabolism are preserved in hypertrophic caveolin-3 knockout hearts.American journal of physiology. Heart and circulatory physiology · 2008Article
- An intracellular motif of GLUT4 regulates fusion of GLUT4-containing vesicles.BMC cell biology · 2008Article
- Ins (endocytosis) and outs (exocytosis) of GLUT4 trafficking.Current opinion in cell biology · 2007Review
- Insulin signaling diverges into Akt-dependent and -independent signals to regulate the recruitment/docking and the fusion of GLUT4 vesicles to the plasma membrane.Molecular biology of the cell · 2006Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisInsulin-stimulated glucose transport requires a signalling cascade through kinases protein kinase (PK) Czeta/lambda and PKB that leads to movement of GLUT4 vesicles to the plasma membrane. The aim of this study was to identify missing links between the upstream insulin-regulated kinases and the GLUT4 vesicle trafficking system. MATERIALS AND
methodsA yeast two-hybrid screen was conducted, using as bait full-length mouse munc18c, a protein known to be part of the GLUT4 vesicle trafficking machinery.
resultsThe yeast two-hybrid screen identified PKCzeta as a novel interactor with munc18c. Glutathione S transferase (GST) pull-downs with GST-tagged munc18c constructs confirmed the interaction, mapped a key region of munc18c that binds PKCzeta to residues 295-338 and showed that the N-terminal region of PKCzeta was required for the interaction. Endogenous munc18c was shown to associate with endogenous PKCzeta in vivo in various cell types. Importantly, insulin stimulation increased the association by approximately three-fold. Moreover, disruption of PKCzeta binding to munc18c by deletion of residues 295-338 of munc18c or deletion of the N-terminal region of PKCzeta markedly inhibited the ability of insulin to stimulate glucose uptake or GLUT4 translocation. CONCLUSIONS/
interpretationWe have identified a physiological interaction between munc18c and PKCzeta that is insulin-regulated. This establishes a link between a kinase (PKCzeta) involved in the insulin signalling cascade and a known component of the GLUT4 vesicle trafficking pathway (munc18c). The results indicate that PKCzeta regulates munc18c and suggest a model whereby insulin triggers the docking of PKCzeta to munc18c, resulting in enhanced GLUT4 translocation to the plasma membrane.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.