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Coupling these two enzymes together will result in a much more efficient oxidative pathway and may go some way to explain why the oxidation of PDI by Ero1 in vitro is a relatively inefficient process (Sevier et al, 2007; Baker et al, 2008; Chambers et al, 2010).
This enhanced exercise capacity was due to more efficient oxidative metabolism during low- and high-intensity exercise and more efficient glycolytic metabolism during high-intensity exercise.
In addition to a more efficient oxidative phosphoryllation, HEK293-P2X7 cells also have a more active glycolytic metabolism.
Furthermore, P2X7R-expressing cells also show an enhanced ER Ca2+ handling, an activated NFATc1 and a more efficient oxidative phosphorylation.
Many cancers preferentially meet their energy requirements through the glycolytic pathway rather than via the more efficient oxidative phosphorylation pathway.
For example, in a rapidly growing tumor tissue, HIF-1 helps hypoxic tumor cells to shift glucose metabolism from the more efficient oxidative phosphorylation to the less efficient glycolytic pathway in order to maintain their energy production (the Warburg effect).
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Underlying the transition from low-energy requiring pluripotency into a cardiac phenotype is a switch in energy metabolism, from anaerobic glycolysis to more efficient mitochondrial oxidative phosphorylation [9], [19], [20].
Most cancer cells rely mainly on aerobic glycolysis to generate the energy needed for cellular processes instead of more efficient mitochondrial oxidative phosphorylation, a phenomenon known as the Warburg effect, resulting in an accelerated rate of glucose consumption with enhanced lactate production regardless of oxygen availability.
The results indicated that glucose was being used preferentially in Myog-deleted mice during low-intensity exercise and suggested that Myog-deleted mice were inherently more efficient in utilizing oxidative metabolism than were wild-type mice.
Both glycolysis and the more efficient mechanism of oxidative phosphorylation contribute to ATP generation in the Drosophila larva.
Since induction of heme oxygenase is a general response to oxidative stress, we suspect that the differential toxicity of arsenic to human and animal cells could be due to arsenic's more efficient induction of oxidative damage in human cells.
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