Positive and negative regulation of insulin signaling through IRS-1 phosphorylation.
By P. Gual, Y. Le Marchand-Brustel, J. Tanti. Biochimie, 2005
920 citations recorded by the source corpus.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/fc5190a8b97a7e0adf74946c21f25cae4ac84402
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- J. Engelman
- Lewis C. Cantley
- A. M. Houghton
- John Q. Trojanowski
- A. Gregory
- M. V. Vander Heiden
- David M. Sabatini
- P. Pandolfi
In Surgery
Citations in the corpus
- Demonstrated brain insulin resistance in Alzheimer's disease patients is associated with IGF-1 resistance, IRS-1 dysregulation, and cognitive decline. (2012, positive): “A well-established, albeit not exclusive (45), cause of insulin resistance in T2D is chronic upregulation of a normally adaptive feedback/feed-forward mechanism that attenuates insulin signaling via phosphorylation of IRS-1 at S312, S616, and/or S636 (equivalent to S307, S612, and S632, respectively”
- The evolution of phosphatidylinositol 3-kinases as regulators of growth and metabolism (2006, background): “JNK-dependent serine phosphorylation inhibits the tyrosine phosphorylation of IRS1, thereby uncoupling IRS1 from PI3K (see below”
- Neutrophil Elastase-Mediated Degradation of IRS-1 Accelerates Lung Tumor Growth (2010, background): “The phosphorylation status of IRS-1 may dictate its behavior, with tyrosine-phosphorylated IRS-1 functioning as a positive effector of growth factor and serine-phosphorylated IRS-1 functioning as a regulatory facto”
- Diabetes associated cell stress and dysfunction: role of mitochondrial and non‐mitochondrial ROS production and activity (2007, background): “This lipid can inhibits phosphatidyl inositol 3-kinase (PI3K), which, in turn, results in a block in protein kinase B (PKB also known as Akt/PKB) activation (Beeharry et al. 2004).”