Title : Manganese superoxide dismutase deficiency triggers mitochondrial uncoupling and the Warburg effect.

Pub. Date : 2015 Aug 6

PMID : 25362851






6 Functional Relationships(s)
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1 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus
2 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus
3 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus
4 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus
5 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus
6 When MnSOD is deficient, superoxide radical and its resulting reactive oxygen species (ROS) activate ligand binding to peroxisome proliferator-activated receptor alpha (PPARalpha), suggesting that the activation of PPARalpha signaling is a major mechanism underlying MnSOD-dependent UCPs expression that consequently triggers the PI3K/Akt/mTOR pathway, leading to increased aerobic glycolysis. Reactive Oxygen Species peroxisome proliferator activated receptor alpha Mus musculus