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https://www.selleckchem.com/products/luzindole.html There is increasing evidence that inducing neuronal mitophagy can be used as a therapeutic intervention for Alzheimer's disease. Here, we screen a library of 2024 FDA-approved drugs or drug candidates, revealing UMI-77 as an unexpected mitophagy activator. UMI-77 is an established BH3-mimetic for MCL-1 and was developed to induce apoptosis in cancer cells. We found that at sub-lethal doses, UMI-77 potently induces mitophagy, independent of apoptosis. Our mechanistic studies discovered that MCL-1 is a mitophagy receptor and directly binds to LC3A. Finally, we found that UMI-77 can induce mitophagy in vivo and that it effectively reverses molecular and behavioral phenotypes in the APP/PS1 mouse model of Alzheimer's disease. Our findings shed light on the mechanisms of mitophagy, reveal that MCL-1 is a mitophagy receptor that can be targeted to induce mitophagy, and identify MCL-1 as a drug target for therapeutic intervention in Alzheimer's disease.An amendment to this paper has been published and can be accessed via a link at the top of the paper.Microbial methanogenesis in anaerobic soils contributes greatly to global methane (CH4) release, and understanding its response to temperature is fundamental to predicting the feedback between this potent greenhouse gas and climate change. A compensatory thermal response in microbial activity over time can reduce the response of respiratory carbon (C) release to temperature change, as shown for carbon dioxide (CO2) in aerobic soils. However, whether microbial methanogenesis also shows a compensatory response to temperature change remains unknown. Here, we used anaerobic wetland soils from the Greater Khingan Range and the Tibetan Plateau to investigate how 160 days of experimental warming (+4°C) and cooling (-4°C) affect the thermal response of microbial CH4 respiration and whether these responses correspond to changes in microbial community dynamics. The mass-specific CH4 r

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