Critical nodes in signalling pathways: insights into insulin action

By C. Taniguchi, Brice Emanuelli, C. Kahn. Nature reviews. Molecular cell biology, 2006

2,830 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/840c03a8aecfaa2f60bca47c079455ac4f06e0a7

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Citations in the corpus

The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, neutral): “[38] Taniguchi CM, Emanuelli B, Kahn CR.”
Inflammation and insulin resistance (2008, background): “The second pathway is the Ras-mitogen activated protein kinase (MAPK) pathway which mediates gene expression, but also interacts with the PI3K-AKT pathway to control cell growth and differentiation (reviewed in [8]).”
Molecular Mechanisms of Insulin Resistance in Humans and Their Potential Links With Mitochondrial Dysfunction (2006, background): “Downstream molecules such as phosphatidylinositol-dependent kinase (PDK) and protein kinase B (PKB [AKT]) have a pleckstrin homology domain that enables these molecules to migrate toward the plasma membrane (28).”
Lipid signalling in disease (2008, background): “Among other substrates, insulin stimulates tyrosine phosphorylation of insulin receptor substrate (IRS”
Metabolic Regulation of Immune Responses (2014, background): “For instance, insulin is the primary signal that mediates the uptake, storage, mobilization, and utilization of fuels in non-immune target cells, such as adipocytes, hepatocytes, and myocytes (1).”
Skeletal Muscle Insulin Resistance Is the Primary Defect in Type 2 Diabetes (2009, background): “This results in activation of downstream protein kinase B (also called Akt) and phosphorylation of Akt substrate 160 (AS160), which facilitates the translocation of GLUT4 to the sarcolemma and subsequent entry of glucose into the cell (25).”
Pathogenesis of non-alcoholic fatty liver disease (2009, background): “These include FFAs, tumour necrosis factor-alpha (TNF-a), nuclear factor kappa B (NF-kB), ceramide, jun N-terminal kinase 1 (JNK1), SOCS (suppressors of cytokine signalling) and cytochrome CYP2E1.(39,40) Increased lipid metabolites such as diacylglycerol (DAG) have been implicated in a protein kinas”
The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism (2006, background): “In mammals, the PI3K–AKT signalling pathway has a central role in the regulation of metabolism downstream of the insulin receptor and IRS adaptor molecules (reviewed in Ref”