Session 2Alteration in insulin action: role of IRS-1 serine phosphorylation in the retroregulation of insulin signallingAnomalies dans l’action de l’insuline : rôle de la sérine phosphorylation d’IRS-1 dans la régulation négative du signal insulinique
Références (41)
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The c-Jun NH2-terminal Kinase promotes insulin resistance during association with Insulin Receptor Substrate-1 and phosphorylation of Ser307
J Biol Chem
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Phosphorylation of Ser307 in insulin receptor substrate-1 blocks interactions with the insulin receptor and inhibits insulin action
J Biol Chem
(2002) - et al.
JNK: a new therapeutic target for diabetes
Curr Opin Pharmacol
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Serine phosphorylation of insulin receptor substrate 1 by inhibitor k B Kinase complex
J Biol Chem
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Modulation of insulin stimulated degradation of human insulin receptor substrate-1 by Serine 312 phosphorylation
J Biol Chem
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Hyperosmotic stress inhibits IRS-1 function by distinct mechanisms in 3T3-L1 adipocytes
J Biol Chem
(2003) - et al.
Positive and negative regulation of glucose uptake by hyperosmotic stress
Diabetes Metab
(2003) - et al.
c-Jun N-terminal kinase (JNK) mediates feedback inhibition of insulin signaling cascade
J Biol Chem
(2003) - et al.
Phosphorylation of the insulin receptor substrate-1 on multiple serine residues 612, 632, 662 and 731, modulates insulin action
J Biol Chem
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A molecular basis for insulin resistance. Elevated serine/threonine phosphorylation of IRS-1 and IRS-2 inhibits their binding to the juxtamembrane region of the insulin receptor and impairs their ability to undergo insulin-induced tyrosine phosphorylation
J Biol Chem
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Phosphorylation of insulin receptor substrate-1 (IRS-1) by protein kinase B positively regulates IRS-1 function
J Biol Chem
Protein kinase C-zeta phosphorylates insulin receptor substrate-1 and impairs its ability to activate phosphatidylinositol 3-kinase in response to insulin
J Biol Chem
Cross-talk between the Platelet-derived Growth Factor and the insulin signaling pathways in 3T3-L1 adipocytes
J Biol Chem
Serine/threonine phosphorylation of insulin receptor substrate 1 modulates insulin receptor signaling
J Biol Chem
Effects of okadaic acid, an inhibitor of proteinphosphatases-1 and -2A, on glucose transport and metabolism in skeletal muscle
J Biol Chem
Mechanism by which fatty acids inhibit insulin activation of insulin receptor substrate-1 (IRS-1)-associated phosphatidylinositol 3-kinase activity in muscle
J Biol Chem
Insulin resistance: a phosphorylation-based uncoupling of insulin signaling
Trends Cell Biol
Reduced activation of phosphatidylinositol-3 kinase and increased serine 636 phosphorylation of insulin receptor substrate-1 in primary culture of skeletal muscle cells from patients with type 2 diabetes
Diabetes
Enhanced basal activation of mitogen-activated protein kinases in adipocytes from type 2 diabetes: potential role of p38 in the downregulation of GLUT4 expression
Diabetes
Impaired glucose transport as a cause of decreased insulin-stimulated muscle glycogen synthesis in type 2 diabetes
N Engl J Med
Cited by (48)
The contribution of gastrointestinal microbiota in the existence of type 2 diabetes in Saudi Arabia: Current information and perspectives
2022, Saudi Journal of Biological SciencesCitation Excerpt :Fagiolo et al. (1993) recorded that cytokine production elevated with age. Moreover, the administration of LPS in rodents has been reported to elevate triglyceride levels by de novo fatty acids synthesis, which have been shown to increase the sein phosphorylation of IRS-1) (Feingold et al., 1992; Tanti et al., 2004) (Fig. 2). Therefore, the gut microbiota appeared to link LPS of plasma, cytokine, inflammation, fatty acids, and insulin resistance.
Disturbances of systemic and hippocampal insulin sensitivity in macrophage migration inhibitory factor (MIF) knockout male mice lead to behavioral changes associated with decreased PSA-NCAM levels
2017, Hormones and BehaviorCitation Excerpt :However, at the molecular level, inhibitory phosphorylation of IRS1 at serine 307 (pIRS1Ser307) represents an early hallmark of insulin resistance leading to impairment of IRS1 ability to activate downstream kinase and transduce insulin signal (Sykiotis and Papavassiliou, 2001). It was previously shown that “diabetogenic” factors such as fatty acids and proinflammatory cytokines may lead to increased inhibitory serine Ser307 phosphorylation of IRS1 (Tanti et al., 2004). The underlying mechanism that links hippocampal insulin resistance and altered behavior could be impaired plasticity of neuronal networks and reduced hippocampal neurogenesis, since insulin is involved in regulation of these processes (Blazquez et al., 2014).
Gut microbiota and immune crosstalk in metabolic disease
2016, Molecular MetabolismCitation Excerpt :Innate immune cells infiltrate the tissues through a mechanism requiring the expression of the C–C motif chemokine receptor-2 (CCR2) by the circulating monocytes tissue macrophages and the production of chemokine ligand-2 (CCL2) and MCP1 by adipose tissue derived cells [27]. Activated M1 macrophages produce large amounts of TNFα, IL-1β, and IL-6, which contribute to insulin resistance by phosphorylating the c-Jun amino terminal kinase (JNK) and inhibitor of nuclear factor kappa B kinase subunit β (IKK-β) responsible for the phosphorylation of serine of IRS-1 [28,29]. Serine phosphorylation inactivates the IRS, which reduces insulin signaling and triggers insulin resistance.
Sustained action of ceramide on the insulin signaling pathway in muscle cells: Implication of the double-stranded RNA-activated protein kinase
2016, Journal of Biological Chemistry