oxidative phosphorylation

All of the above risk factors impact mitochondrial oxidative phosphorylation.

The main function of the intermembrane space is oxidative phosphorylation.

More genes for oxidative phosphorylation are expressed when it is subject to darkness.

They are believed to activate enzymes involved with oxidative phosphorylation.

The overall process of creating energy in this fashion is termed oxidative phosphorylation.

The citric acid cycle is always followed by oxidative phosphorylation.

These reactions and processes are required for oxidative phosphorylation.

Some of these proteins are also essential parts of oxidative phosphorylation.

There are several well-known drugs and toxins that inhibit oxidative phosphorylation.

This structure traps one proton, which is quite helpful for oxidative phosphorylation.

This can damage the entire oxidative phosphorylation system, especially the highly vulnerable iron-sulfur centers.

This process is part of oxidative phosphorylation.

Mitchell's chemiosmotic hypothesis was the basis for understanding the actual process of oxidative phosphorylation.

It mainly acts by uncoupling of Oxidative phosphorylation in flukes.

In oxidative phosphorylation research, it is used to prevent state 3 (phosphorylating) respiration.

Almost all aerobic organisms carry out oxidative phosphorylation.

This is important in driving oxidative phosphorylation.

Until now there have been few reports on hepatic failure caused by disorders of mitochondrial oxidative phosphorylation.

It is one of the "entry enzymes" of oxidative phosphorylation in the mitochondria.

Oxidative phosphorylation in the eukaryotic mitochondrion is the best-understood example of this process.

Not all inhibitors of oxidative phosphorylation are toxins.

DNP is probably the best known agent for uncoupling oxidative phosphorylation.

One of these, rafoxanide, apparently acts by uncoupling oxidative phosphorylation in the fluke.

Instead, processes such as oxidative phosphorylation and photosynthesis take place across the prokaryotic cell membrane.

Class II mitochondrial disorders stem from secondary defects in oxidative phosphorylation.