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. 2017 Feb 27;6(3):e004694. doi: 10.1161/JAHA.116.004694

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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MicroRNA (miR)‐181a/b inhibits PI3K pathway activity in the miR‐181a/b^−/− mouse heart through modulation of phosphatase and tensin homolog (PTEN). Western blot analysis of (A) PTEN, (B) phosphorylation of Akt (pAkt) Ser 473, and total Akt expression in the heart from wild type (WT), miR‐181a/b^−/−, and miR‐181c/d^−/− knockout mice whole‐heart homogenates were probed with the indicated antibodies. α‐Tubulin is a loading control. Band densitometry is shown in the bar graph. C, Quantitative polymerase chain reaction (SYBR kit) analysis of miR‐181 family (a, b, c, and d) expression in total RNA from the heart homogenate of WT mouse hearts. miRNA expression was normalized to 5S r RNA. *P<0.05 vs WT, n=4.