Signaling pathways in insulin action: molecular targets of insulin resistance.

By J. Pessin, Alan R. Saltiel. Journal of Clinical Investigation, 2000

996 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/68ecb8fcca8f87118bc7f3b4acb4a6d4b242638c

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Citations in the corpus

Adipokines Mediate Inflammation and Insulin Resistance (2013, background): “Insulin also increases lipogenesis in hepatocytes and adipocytes and diminishes adipocyte free fatty acid generation from triacylglycerols (lipolysis) (Pessin and Saltiel, 2000).”
Trends in insulin resistance: insights into mechanisms and therapeutic strategy (2022, background): “Insulin is released by pancreatic beta cells and is essential for glucose and lipid homeostasis.(21) Insulin binds the insulin receptor (INSR) on the plasma membrane of target cells, leading to the recruitment/phosphorylation of downstream proteins, that primarily including insulin receptor substrat”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, positive): “In endothelial cells, insulin activates endothelial nitric oxide synthase, resulting in vasodilation (227, 251).”
Pathogenesis of type 2 diabetes mellitus. (2004, background): “Inhibitors of PI3K impair glucose transport and block the activation of glycogen synthase and hexokinase (HK)-II expression [160–162,165,167–169].”
The Fluid-Mosaic Model of Membrane Structure: still relevant to understanding the structure, function and dynamics of biological membranes after more than 40 years. (2014, background): “Then the receptor undergoes a series of intramolecular transphosphorylation reactions in which one subunit of the complex phosphorylates an adjacent subunit of the complex in order to initiate the signaling process [157].”
Molecular and cellular endocrinology (2000, neutral): “Insulin resistance occurs when normal circulating concentrations of the hormone are insufficient to regulate these processes appropriately (Pessin and Saltiel, 2000).”
Insulin-stimulated GLUT4 translocation requires the CAP-dependent activation of TC10 (2001, background): “Activation of phosphatidylinositol-3-OH kinase (PI(3)K) is required for this trafficking event, but it is not sufficient to produce GLUT4 translocatio”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “While Akt is thought to be a central effector driving glucose transport, other signaling cascades are thought to participate in parallel including the aPKCλ/ζ (187, 188, 363), p-38 mitogen-activated protein kinase (622), and the CAP/c-Cbl/ TC10 cascade (57, 500).”
Pathogenesis of Insulin Resistance in Skeletal Muscle (2010, background): “The phosphorylated tyrosine residues of IRS-1 mediate an association with the 85-kDa regulatory subunit of phosphatidylinositol 3-kinase (PI3K), leading to activation of the enzyme [138–140, 143, 144].”