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Autophagy through p62 plays an important role in regulating insulin receptor substrate 1 protein levels in response to nutritional deficiency. The present findings suggest that autophagy might function as energy depletion-sensing machinery that finely tunes insulin signal transduction.
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CD36 functioned through ubiquitination-dependent binding to IRS1 and inhibiting its interaction with cullin 7.
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this study shows that microRNA-126 deficiency enhanced the activation and function of CD4(+) T cells by elevating IRS-1 pathway
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The data suggest that upregulated Irs1 by Wnt3a/beta-catenin signaling plays a crucial role in the progression of hepatocellular carcinoma.
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DPP-4 inhibitor sitagliptin has effects on cardiac function, glycemia, and beta-cell function together with reducing S6K1 activation and IRS-1 and IRS-2 degradation in the obesity female mouse model
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'selective insulin resistance' is caused by the differential expression of Irs1 and Irs2 in different zones of the liver
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Lung-specific dual ablation of insulin receptor substrates 1/2 (succumb to tumor burdenIrs1/Irs2) strongly suppresses tumor initiation and dramatically extends the survival of a mouse model of lung cancer with Kras activation and p53 loss. Mice with Irs1/Irs2 loss eventually.
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Noise exposure led to enhanced JNK phosphorylation and IRS1 serine phosphorylation as well as reduced Akt phosphorylation in skeletal muscles in response to exogenous insulin stimulation.
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The data, therefore, suggest that 1,25(OH)2D3 increases glucose consumption by inducing SIRT1 activation, which in turn increases IRS1 phosphorylation and GLUT4 translocation in myotubes.
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Results show that lack of IRS1 prevents beta-cell apoptosis induced by ER stress, and promotes XBP-1 instability secondary to proteasomal degradation.
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Using two long-lived IIS models, namely Drosophila lacking three insulin-like peptides (dilp2-3,5(-/-)) and mice lacking insulin receptor substrate 1 (Irs1(-/-)), and two independent translation assays, polysome profiling and radiolabeled amino acid incorporation, we show that reduced IIS lowers translation in these organisms
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findings suggest that up-regulation of miR-222 followed by reduction in IRS-1 expression may be a viable mechanism of insulin resistance in the liver
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These results demonstrate the cooperative interaction between RPTPbeta and the IGF-I receptor leading to a coordinated series of signaling events that are required for osteoblast differentiation. Our findings emphasize the important role IRS-1 plays in modulating these signaling events and confirm its essential role in facilitating osteoblast differentiation
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EGCG significantly ameliorated insulin resistance and cognitive disorder by up-regulating the insulin receptor substrate-1 (IRS-1)/AKT and ERK/cAMP response element binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathways.
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Pit1 deletion inhibited USP7/IRS1 dissociation upon insulin stimulation.
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TSH improves insulin sensitivity in skeletal muscle by increasing Irs1 gene expression.
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Insulin receptor substrate-1 time-dependently regulates bone formation by controlling collagen Ialpha2 expression via miR-342
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Irs1 was downregulated in the arcuate nucleus of type 2 diabetic mice.
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In conclusion, we have identified that ARL15 acts as an insulin-sensitizing effector molecule to upregulate the phosphorylation of members of the canonical IR/IRS1/PDPK1/AKT insulin pathway by interacting with its GAP ASAP2 and activating PDPK1. This research may provide new insights into GTPase-mediated insulin signalling regulation and facilitate the development of new pharmacotherapeutic targets for insulin sensitizati
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These findings illuminate a new function of IRS-1: that of maintaining cells in their normal, differentiated state. Because IRS-1 is down-regulated in states of insulin resistance that occur in response to metabolic stresses such as obesity and cytokine stimulation
