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This study found that in a mouse model of Leigh syndrome, rapamycin alters brain proteome and may extend survival by targeting protein kinase C.

Martin-Perez et al. show that rapamycin's beneficial effects in a mouse model of Leigh syndrome are linked to the downregulation of protein kinase C.

In this study, researchers found that mitochondrial complex I plays a crucial role in regulating innate immunity and bone remodeling, with Ndufs4 deletion causing systemic inflammation and osteopetrosis through various metabolic shifts and cellular mechanisms.

This study found that conditional deletion of Mof in mice resulted in severe defects in skin development, including compromised epidermal differentiation and hair growth, leading to perinatal lethality.

This study found that FLCN deficiency in mice muscles led to increased mitochondrial biogenesis and a metabolic shift towards oxidative phosphorylation, with a similar advantage observed in FLCN-null kidney cancer cells.