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. 2011 Dec 27;44(4):259–267. doi: 10.1152/physiolgenomics.00173.2011

Fig. 3.

Fig. 3.

Kallikrein 5 (KLK5) was targeted by miR-382. A: miR-382 knockdown did not have significant effects on epithelial mesenchymal transition (EMT) markers E-cadherin or α-smooth muscle actin (SMA) expression. Anti-scramble-treated n = 10/group, anti-miR-382 n = 8/group. #P < 0.05 vs. sham-operated animals receiving the same anti-miR treatment. B: the mRNA expression of several predicted miR-382 targets implicated in extracellular matrix remodeling. KLK5 expression was significantly increased when miR-382 was knocked down in sham-operated animals. *P < 0.05 vs. anti-scrambled treated mice with same surgery (P < 0.05). C: MicroCosm-predicted binding site within the 3'-untranslated region (UTR) of mouse KLK5. The seed region is boldfaced and underlined, with wobble pairs represented by curved lines. 3′-UTR reporter analysis confirmed an interaction between miR-382 and the 3′-UTR of KLK5. This interaction did not occur when a point mutation was introduced to the seed region binding sequence by inversion of the “AC” nucleotides (framed by box). n = 4–8 for anti-miR-treatment; n = 10–12 for pre-miR-treatment. *P < 0.05 vs. control oligonucleotides.

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