In addition to increasing glycolysis, some proliferating cells exhibiting the Warburg effect also increase oxidative phosphorylation through mitochondrial fusion.

Biochemical analyses show that mitochondrial COX16 assists in the process of copper insertion into COX2 and reveal a second COX16 function in linking assembly routes of the redox center-containing COX1 and COX2 subunits.

Interactions between Aim24 and the mitochondrial outer and inner membrane contact site complex (MICOS) are essential for mitochondrial ultrastructure, lipid composition and oxidative phosphorylation.

NFATc2 maintains the drug-induced TIC phenotypes through trans-activating SOX2/ALDH1A1 expression and scavenging stress from ROS.

Analysis of aging yeast cells using the in-vivo roGFP2-based probe reveals redox-dependent heterogeneity, reflected in a bi-modal distribution of the oxidation status, differential growth and replication, as well as distinct proteomic and transcriptomic profiles.

Excitotoxicity driven by NMDA receptor hyper-activation does not involve DAPK1-dependent events in vitro or in vivo, and previously described DAPK1-NMDAR disrupting peptides act by blocking the NMDA receptor.

The development of diet-dependent obesity results in the deterioration of calcium homeostasis in pro-opiomelanocortin-expressing neurons and impaired function of the same neurons.