Diagram of mitochondrial oxidative phosphorylation showing the major Biology Diagrams Abstract. Mitochondria play an essential role in oxidative phosphorylation, fatty acid oxidation, and the regulation of apoptosis. However, this organelle also produces reactive oxygen species (ROS) that continually inflict oxidative damage on mitochondrial DNA, proteins, and lipids, which causes further production of ROS.
Shin et al. report that ATP-linked mitochondrial respiration controls the Th17 and Treg cell fate decision by supporting TCR signaling and Th17-associated molecular events. Inhibition of mitochondrial OXPHOS ablates Th17 pathogenicity in a mouse model of MS and results in generation of functionally suppressive Treg cells under Th17 conditions. Sustained cellular function and viability of high-energy demanding post-mitotic cells rely on the continuous supply of ATP. The utilization of mitochondrial oxidative phosphorylation for efficient
Control mechanisms in mitochondrial oxidative phosphorylation Biology Diagrams
The model is for oxidative phosphorylation in intact cells and tissues rather than preparations of isolated mitochondria. Mitochondria are extensively damaged during isolation and this damage, combined with the use of non‐physiological assay conditions, yields data that can be very misleading if interpreted out of context. This fact supports the role of mitochondria in biochemical requirements of highly proliferative neuronal stem cells and post-mitotic neurons. During neuronal differentiation, the number of mitochondria per cell increases, Oxidative phosphorylation in cells is not fully efficient. Decrease of the proton gradient across the inner
Oxidative stress is known to induce cell cycle arrest, but the effects of ROS on the cell cycle, especially mitotic progression, are not fully understood. Cdc25C, a phosphatase that removes inhibitory phosphorylation from Cyclin B/Cdk1, is sensitive to oxidation.
Oxidative stress induces mitotic arrest by inhibiting Aurora A Biology Diagrams
Distinct roles have been demonstrated for mitochondrial fission and fusion in different cancer contexts. Targeting of factors mediating mitochondrial dynamics may be directly related to impairment of oxidative phosphorylation, which is essential to sustain cancer cell growth and can also alter sensitivity to chemotherapeutic compounds.
