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"In addition, Nrf2 deletion impaired Otud1 ability in reducing pro-apoptotic proteins and elevating anti-apoptotic protein Bcl2 in H/R-stimulated primary hepatocytes (Fig. S7A)."

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"These findings indicate that OTUD1 attenuates mitochondria damage caused by oxidative stress following H/R treatment in vitro.2.4 OTUD1 mitigates hepatocyte H/R injury by activating NRF2/ARE pathway."