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The protein-protein docking study of SOCS1 with its natural substrates, IRS1 and IRS2, and subsequent solvent accessible surface area analysis gave insight into the binding region of the SOCS1 protein.
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The report the association between common variants in IRS1 gene with insulin resistance, glucose, and HbA1c levels in Bosnia and Herzegovina's population.
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The decreased hepatic expression of IRS1 and beta-catenin in nonalcoholic fatty liver disease is linked to histological progression such as ballooning, and might lead to diabetes as a result of impaired glucose metabolism.
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the expression level of miR-466 was significantly downregulated in tumor tissues and cell lines, and its overexpression was able to inhibit cell proliferation and invasion. The tumor-suppressive roles of miR-466 in OS cells were mediated by the silencing of IRS1.
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Studied insulin resistance in human nonalcoholic fatty liver disease patients and controls by analyzing gene expression levels of molecules involved in insulin signaling including insulin receptor substrate 1(IRS-1) and insulin receptor substrate 2(IRS-2).
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miR-30e blocked the activation of AKT and ERK1/2 pathways, and the expression of HIF-1alpha and VEGF via directly targeting IRS1.
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Adipose tissue DNA promoter methylation correlated negatively with insulin receptor substrate 1 IRS-1 (IRS1) gene expression in obese subjects.
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The presence of AA genotype in both CCR5 59029 and IRS1 rs10498210 is associated with type 2 diabetes.
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This study establishes a new role for IRS-1 as an endocytic regulator of IGF-IR that ensures sustained IGF bioactivity, independent of its classic role as an adaptor in IGF-IR signaling.
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Overexpression of IRS-1 protein is associated with expression of p-Akt, and could be an independent biomarker for poor prognosis in breast invasive ductal carcinoma.
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miR-664 is downregulated in BC tissues and cell lines. In addition, miR-664 restricts proliferation and migration of BC cells. Moreover, IRS1 is validated as a direct target of miR-664 in BC.
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Neither the PPARgamma nor the IRS-1 polymorphism was associated with mortality outcome in breast-cancer patients. The TNF-alfa -308 G > A polymorphism was associated with reduced breast-cancer-specific and all-cause mortality.
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Results show that ectopic expression of SH2B1 in lung adenocarcinoma (LADC) cell line H1299 cells increased IRS1 expression level. Reduced expression of IRS1 considerably inhibited H1299 cell proliferation, migration, and invasion. These findings suggest that IRS1 plays a role in LADC carcinogenesis.
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Axl binds to and phosphorylates TNS2 and that Axl/TNS2/IRS-1 cross-talk may potentially play a critical role in glucose metabolism of cancer cells.
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our present data point to IRS1 rs1801278 as a potential biomarker for pursuing the goal of stratified medicine in the field of antihyperglycemic treatment in type 2 diabetes .
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IRS-1 gene polymorphism Gly972Arg was found a significant risk factor for ischemic stroke in Indonesian subjects.
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ER and IRS-1 subgroups appear to be critical factors for the prediction of breast cancer recurrence. In particular, we suggest that the patients who have ER-positive and IRS-1-negative breast cancer undergo more aggressive treatment because they have poorer prognoses.
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our findings suggested that the overexpression of LncRNA H19 could inhibit cell proliferation and promoted apoptosis via downregulation of IRS-1 in thyroid cancer cells in vitro. These findings might provide important clues for the establishment of LncRNA H19 functional network in thyroid cancer. Long noncoding RNA H19 might be a potential new target for antitumor therapy of thyroid cancer
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Acute loss of IRS1/IRS2 or inhibition of IR/IGF1R in KRAS-mutant human NSCLC cells decreases the uptake and lowers the intracellular levels of amino acids, while enhancing basal autophagy and sensitivity to autophagy and proteasome inhibitors.
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S6K1-dependent IRS-1pSer suppresses insulin signaling leading to insulin resistance, which is frequently observed in AD brains. Notably, miR-200b/c transfection of SH-SY5Y cells reduced the levels of IRS-1pSer. This finding indicates that miR-200b/c has the potential to alleviate insulin resistance via modulation of S6K1