Metabolic Regulation, Mitochondria and the Life-Prolonging Effect of Rapamycin: A Mini-Review | Zendy

Yong Pan | Zendy; Yuya Nishida | Zendy; Margaret Wang | Zendy; Eric Verdin | Zendy

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Metabolic Regulation, Mitochondria and the Life-Prolonging Effect of Rapamycin: A Mini-Review

Author(s) -

Yong Pan,

Yuya Nishida,

Margaret Wang,

Eric Verdin

Publication year - 2012

Publication title -

gerontology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.397

H-Index - 94

eISSN - 1423-0003

pISSN - 0304-324X

DOI - 10.1159/000342204

Subject(s) - tor signaling , mitochondrial biogenesis , effector , mitochondrion , microbiology and biotechnology , biology , nutrient sensing , biogenesis , kinase , serine , signal transduction , mtorc1 , metabolism , cellular metabolism , mechanistic target of rapamycin , autophagy , phosphorylation , pi3k/akt/mtor pathway , biochemistry , apoptosis , gene

The fungicide rapamycin increases lifespan in eukaryotes by interfering with the activity of a serine/threonine kinase called TOR (target of rapamycin). TOR complex 1 (TORC1) is an essential integrator of cellular nutrient cues, growth signals and cellular metabolism. Here, we review major components of TORC1, its downstream effectors and lifespan studies in various organisms involving these signaling components. In particular, we focus on the role of rapamycin in mitochondrial biogenesis, in metabolic regulation and in the control of reactive oxygen species production.

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