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Longevity Briefs: Starvation-induced molecular mechanisms: paradox resolution.

Posted on 2 October 2020

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Longevity briefs provides a short summary of a novel research, medicine, or technology that caught the attention of our researchers in Oxford, due to its potential to improve our health, wellbeing, and longevity.

Why is this research important: Our bodies have developed a mechanism through evolution, that reduces protein synthesis during starvation periods. However, activation of starvation-induced mechanism does require protein synthesis, conflicting with global protein synthesis reduction. It is unclear how said conflict is resolved and it is crucial in the understanding of cell health.

What did the researchers do: In this article, researches have analysed transcription of the genome for protein synthesis in the presence of transcription factor EB (TFEB). TFEB was chosen because it is translocated to the nucleus during inhibition of the mammalian target of rapamycin complex 1 (mTORC1) and inhibition of mTORC1 takes place during starvation.

Key takeaway(s) from this research: It was shown that TFEB increases early expression GADD34, which in turn prevents excessive phosphorylation of eukaryotic translation initiation factor 2 (eIF2α). This allows the translation of starvation-induced mechanisms. Also, this research has shown that both excess and under phosphorylation of eIF2a negatively impact a cell’s metabolism. This raises a question of how the optimal level of eIF2a is determined and the answer can potentially be beneficial in disorders that include starvation-induced mechanisms.

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