Abstract
The ectopic expression of miR-15b is linked causally to impaired insulin signaling in human HepG2 hepatocytes through the suppression of INSR (Yang et al., 2015) [1]. In this data article, we further examined the effect of miR-15b on insulin signaling in a murine skeletal muscle cells, C2C12 myocytes. Although the 3’UTR of mouse INSR mRNA has an appropriate binding site for miR-15b based on TargetScan analysis, the ectopic expression of miR-15b did not suppress the expression and insulin-stimulated phosphorylation of insulin signaling intermediates in C2C12 myocytes. A more detailed understanding of the effects of miR-15b on hepatic insulin resistance can be found in “Obesity-induced miR-15b is linked causally to the development of insulin resistance through the repression of the insulin receptor in hepatocytes” (Yang et al., 2015) [1].
Highlights
The ectopic expression of miR-15b is linked causally to impaired insulin signaling in human HepG2 hepatocytes through the suppression of INSR (Yang et al, 2015) [1]
We further examined the effect of miR-15b on insulin signaling in a murine skeletal muscle cells, C2C12 myocytes
The 3’UTR of mouse INSR mRNA has an appropriate binding site for miR-15b based on TargetScan analysis, the ectopic expression of miR-15b did not suppress the expression and insulin-stimulated phosphorylation of insulin signaling intermediates in C2C12 myocytes
Summary
The anti-IRS-1 antibody was purchased from Upstate Biotechnology (Lake Placid, NY, US), and the antibody against phospho-IRS-1 (Tyr632) and β-actin were supplied by Santa Cruz Biotechnology (Santa Cruz, CA, US). The antibodies against INSR, phospho-INSR (Tyr1361), Akt, phospho-Akt (Ser473) were obtained from Cell Signaling Technology (Danvers, MA, US). ECL Western Blotting Detection Reagents from GE Healthcare (Buckinghamshire, UK) were used to visualize the immunoblot. All other chemicals and materials were purchased from Sigma
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