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Similarly, Insulin-like growth factor 1 hair cell protection from neomycin damage is lost by inhibition of Akt or MEK signaling, suggesting that growth factor otoprotection may operate on a similar set of downstream targets (Hayashi et al., 2003

It has been shown that DPP III competes with NRF2 to interact with KEAP1 ubiquitin ligase, thus blocking the ubiquitination of NRF2, leading to NFR2 mediated uncontrolled transcriptional activation especially in squamous cell lung carcinoma 7

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