The suppression of the activity of a specific protein C/EBPβ-LIP slows aging in mice and increase life expectancy in animals.
An international group of scientists has found that suppressing the activity of specific protein C/EBPβ-LIP slows aging in mice and increase life expectancy in animals. Preprint of a study published in the repository bioRxiv.
It is known that the inhibition of using rapamycin protein complex mTORC1 (eng. mammalian target of rapamycin complex 1), involved in the regulation of protein synthesis, allows you to extend the life of various animal species. In humans, however, this approach is difficult since the suppression of the activity of mTORC1 can cause unwanted side effects. Therefore, researchers are looking for other ways through which you can safely affect the protein complex.
According to scientists, a target for drugs may be a transcription factor (activator genes) C/EBPβ. This compound is involved in providing a metabolism of liver and adipose tissue. The gene responsible for the synthesis of this protein may also encode two isoforms of C/EBPβ — Liver Activator Protein (LAP) and Liver-enriched Inhibitory Protein (LIP). The latter compound is synthesized under the influence of mTORC1, which shifts the reading frame to.
Reading frame is composed of a sequence of triplets of nucleotides, each of which encodes a particular amino acid. The shear frame by one nucleotide forward or back alters the composition of the triplets and hence the sequence of amino acids in the corresponding protein.
With aging, the content of the LIP relative to the LAP increases, however, scientists have shown that in mutant mice in which the shift of the reading frame was crushed, the LIP in old age remains low, and life expectancy increased. According to scientists, it is possible to inhibit the synthesis of Liver-enriched Inhibitory Protein in humans.
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