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Closer am1 and am4

autor vlachy 19.Červen 2020

Closer am1 and am4.

„Am1 is t카지노 블로그he protein that gets broken down on the mitochondria, and the am4 protein is what gives them their ‚hibernation‘ effect,“ says Sood. „The mitochondria are actually very flexible and can turn out different proteins depending on the needs of the cells, which is why different mitochondria have different functions and have dif마닐라 카지노 여자ferent activities.“

The researchers took advantage of the fact that the proteins that break down am2 also break down its brother, am3, which is thought to be the dominant regulator of mitochondrial activity and efficiency. They also added a small amount of an enzyme called P2X10C to these mitochondria. The P2X10C was produced by the enzyme tyrosine kinase 2C (TEK2C). Sood and his team found that the protein synthesis that follows P2X10C was slower in mouse and rat mitochondria than in human and human and rat liver mitochondria.

„We know that mice get up to 10% fewer peroxidase and SIRT1 proteins and mitochondria have a lower ability to cope with oxidative stress. This study shows that p2X10C is also less efficient in mitochondria,“ says Sood.

Sood and his colleagues are now investigating this idea further. He is also interested in whether the enzymes that break down mitochondrial proteins can be developed or targeted to other metabolic-related pathways in the brain.

„We want to do experiments to investigate if the enzyme p2X10C can be combined with e우리카지노계열nzymes called mitochondrial-targeting proteins, to identify specific sites for activation which could make mitochondria more efficient and have the potential to address some of the diseases such as Alzheimer’s,“ he says.

Sood’s next step will be to investigate whether, in addition to the possible health benefits of such an engineered enzymes, mitochondrial proteins could play a significant role in preventing and slowing disease progression. The researchers are also investigating whether the enzyme p2X10C could be used to target a particular gene responsible for mitochondrial damage and aging. „We are now developing a method that allows us to directly treat mitochondrial dysfunction in mice so that we can then investigate this relationship in humans and see whether p2X10C can slow disease onset, reduce oxidative stress or enhance mitochondrial function or function in multiple diseases,“ he says.

Explore further: Inhibiting mitochondrial oxidative damage via p2X10C in vivo

More information: The study is: A single