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Selman, C. et al. Evidence for lifespan extension and delayed age-related biomarkers in insulin receptor substrate 1 null mice.
Mercken, E. M. et al. SIRT1 but not its increased expression is essential for lifespan extension in caloric-restricted mice.
SFA-1 is specifically required for lifespan extension both by dietary restriction, and modulation of TORC1 pathway components.
Besides, Ot B also requires SIR-2.1 and CLK-1 which is an enzyme in ubiquinone synthesis, for lifespan extension.
In addition, Ot B also requires SIR-2.1 and CLK-1 which is an enzyme in ubiquinone synthesis, for lifespan extension.
Therefore AMPK is not required for lifespan extension by BDR in C. elegans.
If a specific pathway were required for lifespan extension by CIN, then CIN would be unable to prolong lifespan in that mutant.
Pnc1 synthesizes nicotinic acid from nicotinamide [26], which inhibits the NAD+-dependent histone deacetylase Sir2p [27] required for lifespan extension [27] [30].
Sir2 is required for lifespan extension in Saccharomyces cerevisiae [22] and Drosophila melanogaster [6] when exposed to caloric restriction (CR).
The average lifespan of worms fed with smg-2, smg-4, smg-5 or smg-7 RNAi clones was not significantly increased (Table 1), suggesting that NMD inactivation may not be responsible for lifespan extension.
This sentiment was further supported by fascinating evidence suggesting that elevated mitochondrial superoxide levels may actually be required for lifespan extension in some ETC mutant strains [34].
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