The protein phosphatase 6 subunit SAPS3 modulates lifespan by regulating metabolism.

Ying Yang, Da Eun Kang, Qi Fan, Eric A Hanse, Hosung Bae, Rocio A Barahona, Xiyu Shen, Bryan I Ruiz, Shelly H Lee, Katherine R Pasterczyk, Nainpriya Babbar, Katherine G Waldvogel, Roberto Tinoco, Kim N Green, Qin Yang, Cholsoon Jang, Mei Kong

Department of Molecular Biology and Biochemistry, Charlie Dunlop School of Biological Sciences, University of California, Irvine, Irvine, CA 92697, USA. · pubmed

Paper

Abstract

Aging is characterized by disruptions in metabolic homeostasis, yet the mechanisms that regulate these metabolic changes remain poorly understood. We show that the serine/threonine-protein phosphatase 6 (PP6) regulatory subunit 3, SAPS3, is a critical regulator of metabolism during aging. SAPS3 deletion significantly extends lifespan in mice and counteracts age-related impairments in metabolic health. SAPS3 deficiency improves the effects of aging on the affective behaviors, cognition, and motor functions in aged mice. We find that SAPS3 expression is increased during aging to inhibit adenosine monophosphate-activated kinase (AMPK) activity. Deletion of SAPS3 leads to AMPK activation and reverses cellular senescence and aging-induced metabolic alterations. Using in vivo U-

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Research summary

The paper claims that deletion of the SAPS3 protein extends lifespan in mice by activating AMPK and improving metabolic health. This research is relevant as it addresses mechanisms that regulate metabolic changes during aging, potentially offering insights into lifespan extension and age-related health improvements.

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