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IRS1 decreases the amount of IRS1. 19 / 21
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"Thus, our findings suggested that tyrosine nitration of IRS-1 might also contribute to insulin resistance as does serine phosphorylation of this protein.We found a decrease of the IRS-1 protein level [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In the present study, bioinformatics analyses and luciferase assays were employed to show that miR-466 was able to directly target the 3 '-untranslated region of insulin receptor substrate 1 (IRS1) gene, negatively regulating the mRNA and the protein expression levels of IRS1 in OS cells."

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"Regarding the upstream components of the pathway, the sources of significant variance detected by two-way ANOVA tests were due to similarly elevated levels of insulin receptors (Figure 5A), IGF-1 receptors (Figure 5D), and p/T IRS-1 (Figure 5I), and reduced expression of pY-Insulin receptors (Figure 5B), p/T Insulin (Figure 5C) and IGF-1 (Figure 5F) receptors, and IRS-1 (Figure 5G) in CS and ES relative to CC and/or EC."

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"Insulin receptor substrate 1 (IRS1) is a key cytoplasmic adaptor protein crucial for signal transmission downstream of the receptor and treatment with 0.1 µg/l and 1 µg/l CCN4 decreased IRS1 protein expression by 50%, suggesting the direct inhibitory effect of CCN4 on insulin cascade in human skeletal muscle cells [174]."

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"For IRS-1, it was only SYR that further reduced the expression of IRS-1 significantly (p < 0.05) by 16.33% (SYR/NDMA) compared with NDMA alone (Fig. 7C), while both SYR and ASC were able to further decrease the mRNA level of VEGF-α significantly by 6.48% (SYR/NDMA) and 11.03% (ASC/NDMA) respectively compared with NDMA only (Fig. 7D).3.10 Effect of SYR and ASC treatments on mRNA expressions of lung PTEN, FoxO1 and TSC2."

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"Therefore, we further revealed that miR-96 targets 3 ' UTRs of INSR and IRS-1 genes directly to suppress the expression of the INSR and IRS-1 protein, resulting in impaired insulin signaling and glycogen synthesis."

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"Studies have shown that higher IGF-1levels cause a decrease in IRS-1 expression via post-transcriptional modification and by ligand-mediated degradation of IRS-1 via the ubiquitin-mediated 26S proteas[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"This study showed that (i) the expression of miR-1271 in hepatocytes is upregulated by palmitate; (ii) miR-1271 targets INSR and IRS-1 3 ' UTRs directly and downregulates the expression of INSR and IR[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"These data suggest that miR-126 directly targets IRS-1 3 ' UTR and suppresses IRS-1 expression at the posttranscriptional level."

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"With regards to protein synthesis, although either CUR or cycloheximide repressed global protein synthesis, CUR, but not cycloheximide, significantly decreased IRS-1 abundance suggesting CUR lowered I[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Mechanistically, insulin receptor substrate 1 (Irs1) is a direct target of miR-191, and dysregulated IRS1 expression antagonizes STAT5 activation."

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"The reduction of IRS1 after treatment with arsenic for 3 days may trigger IRS1 expression to compensate for the loss."

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"Downregulation of IRS-1 by IRS-1 siRNA decreased IRS-1 levels as expected and also the levels of phosphorylated GSK-3beta, which is downstream from IRS-1 in signal transduction."

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"Transfection of IRS-1 siRNA efficiently reduced the level of IRS-1 in three lung cancer cell lines (i.e., A549, H157 and Calu-1) as detected by Western blotting (XREF_FIG A)."

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"IRS-1 siRNA specifically inhibited the expression of IRS-1 but not IRS-2, -3 and -4."

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"Decreased levels of insulin receptor substrates IRS-1 and IRS-2 levels were observed in neurons, and increased levels of inactivated phospho (Ser )IRS-1 and phospho (Ser )IRS-1 (Moloney et al., 2010)."

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"Our results showed that IRS1 short hairpin RNAs can effectively suppress the expression of IRS1, and inhibit the phosphorylation of AKT in IRS1 pathway; reduce the expression of MMP2, MMP3, MMP13, and MMP14, decrease the expression of TNFRSF11B and RANKL (also known as tumor necrosis factor (ligand) superfamily, member 11), however increase the RANKL and TNFRSF11B ratio; decrease cell survival, proliferation, and mineralization, and impair the differentiation of MC3T3-E1 cells."

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"In these cells, melatonin increases IRS-1 and GLUT4 expression while decreasing p-IRS-1 (Ser307) expression."

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"Also, upon the activation of JNK, the interaction of IRS-1 (insulin receptor substrate 1) with PP4 causes the decreased expression of IRS-1 and increased phosphorylation of IRS-1."