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. 2016 Mar 24;291(20):10625–10634. doi: 10.1074/jbc.M116.713768

FIGURE 5.

FIGURE 5.

MiR-291b-3p mediates cellular lipid accumulation by directly targeting AMPKα1. A, bioinformatics-predicted binding sites of miR-291b-3p in the 3′-UTR of AMPKα1. B, luciferase activity in HEK 293T cells co-transfected with a miR-291b-3p mimic and pmir-GLO (Promega) or pmir-GLO-AMPKα1 3′UTR. C and D, levels of AMPKα1, total AMPK, AMPK phosphorylated at threonine 172 (p-AMPK), total ACC1 and p-ACC1 in NCTC1469 cells transfected with a miR-291b-3p mimic (C) or miR-291b-3p inhibitor (D). E and F, levels of AMPKα1, total AMPK and p-AMPK in the livers of C57BL/6J mice treated with Ad-291m (E) or HFD-fed mice treated with Ad-291i (F). G, expression and phosphorylation of AMPKα1 in NCTC1469 cells treated with an AMPKα1 siRNA. H and I, intracellular triglyceride content (H) and protein levels of p-ACC1 and total ACC1 (I) in NCTC1469 cells treated with a miR-291b-3p inhibitor and the AMPKα1 siRNA. n = 3 independent experiments. *, p < 0.05 (versus NC); **, p < 0.01(versus NC); ***, p < 0.001 (versus NC).