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Buck researchers discover mitochondrial protein that can increase lifespan


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Buck Institute scientists have discovered a new mechanism of how mitochondria start to go wrong.

"... we open a completely different way to think about, measure, mitigate and reverse that process,” said Buck Fellow Chuankai (Kai) Zhou.

Mitochondria- “powerhouse” of the cell, as they provide the units of energy that every cell needs to function.

Growing body of evidence indicates that this dysfunction contributes to aging in general. 

Zhou’s team found an interesting function of a conserved receptor molecule on the surface of mitochondria called Tom70.

It coordinates two steps of biogenesis by regulating the transcriptional activity of mitochondrial proteins inside nucleus.

Amount of protein created must be fine-tuned to meet the needs and import capacity of the mitochondria.

The two processes of communication about needs and uptake into the mitochondria had not been previously linked.

Research by Buck Institute, published in eLife.

In yeast, increasing Tom70 delays ageing related mitochondrial dysfunction

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Independent biomedical research institute focused on aging


Buck Fellow at Buck institute - studies mechanisms underlying the cellular aging process


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