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Talk:Atpenin A5

From Bioblast

{{MitoPedia |description=Atpenin A5 AA5 is a potent and specific inhibitor of Complex II (CII).It binds to the Q-site of CII and was largerly unaffected by the redox state of the Q- junction and the activity of other ETS inhibitors [7] in the presence of sub-saturated level of succinate. Inhibition of CII by AA5 resulted in the elevation of ROS generation [8]. Upon binding of AA5 to the Q-site of CII, the transfer of electrons is blocked and upstream redox-groups including the FAD+ become reduced. The source of ROS could be the FADH2, when the dicarboxylate binding site is unoccupied. Under this circumstance O2 can accept electrons from FADH2 to form superoxide. Elevating the succinate concentration will lead to an increase of the FADH2 level, which is the prerequisite of ROS formation by CII. However, at the same time the dicarboxylate-binding site is occupied by succinate, which arrest ROS production because of the inhibition of the O2 access towards FADH2. Therefore, the netto ROS generation is determined by these two adverse effects. Binding of fumarate can avoid the ROS production of CII. According to Wojtovich AA5 (1 nM) is able to activate the mK(ATP) channel and protects against simulated ischemia-reperfusion (IR) injury in isolated cardiomyocytes [9]. According to the paper of Siebels et al. 250 nM is the required concentration for initiating ROS by CII. |info=[[https://pubmed.ncbi.nlm.nih.gov/19242645/%7C https://pubmed.ncbi.nlm.nih.gov/23800966/ }}

MitoPedia topics: Inhibitor