https://www.selleckchem.com/MEK.html
Furthermore, in LPS‑induced renal tubular epithelial cells (TECs) injury model, that upregulation of miR‑93 was found to attenuate the apoptosis and inflammatory response, as well as reactive oxygen species generation. Mechanistically, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) was identified as a target of miR‑93. Further experiments revealed that LPS‑induced the decrease of phosphorylated (p)‑AKT and p‑mTOR protein expression in vitro are reversed by the overexpression of miR‑93. The results of the present study suggested that
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