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. 2021 Jan 1;11(3):1079–1099. doi: 10.7150/thno.49354

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Prkab1 activated AMPK to promote the oxidation and suppress the synthesis of fatty acid. (A-C) qRT-PCR analysis of Prkab1, Prkaa1 and Prkaa2 expression in FL83B cells upon transfection with si-Prkab1 or OE-Prkab1. (D, E) Western blot analysis of protein levels of Prkab1, Prkaa1 and Prkaa2 in FL83B cells after transfecting with si-Prkab1 or OE-Prkab1. (F) Western blot analysis of phosphorylated AMPK and ACC in FL83B cells with OE-Prkab1, compound C or OE-Prkab1 + compound C treatment. (G) Western blot analysis of phosphorylated AMPK and ACC in FL83B cells with A769662, si-Prkab1 or A769662 + si-Prkab1 treatment. (H) qRT-PCR analysis of lipogenesis-related genes expression in FL83B cells when transfected with si-Prkab1 or OE-Prkab1. (I) ACC activity assay of FL83B cells upon treatment of si-Prkab1 or OE-Prkab1. Error bars represented mean ± s.e.m of 3 independent repeat experiments. *P <0.05, **P <0.01, ***P <0.001.