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1989;21(3 Pt 2):638-644
We first validated the buffering phenotype in the follow-up studies, in which SLC25A19 exhibited milder growth fitness defect compared to the control cells in the presence of complex III inhibitor antimycin, complex I inhibitor piericidin and complex V inhibitor oligomycin than in the regular culture condition (Supplementary Fig
A new approach to polycystic ovary syndrome: The gut microbiota
PINK1/Parkin-dependent mitophagy efficiency decreases, the RAB7/CCZ1-MON1 complex activity is impaired, and autophagosome formation may be blocked, resulting in continued accumulation of damaged mitochondria and protein aggregates [130]
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