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CRON4healthyfuture
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 Posted: Tue Mar 21, 2006 9:53 am Post subject: Various theories of aging converge on AMPK in worms |
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An upcoming paper in Aging Cell has been posted at their Online Early page, and they found that the worm equivalent of mammalian AMPK is a point of intersection between Sir2 and Insuiln/IGF-I signaling, as well as mitochondrial physiology.
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| "We have shown previously that over-expression of an AMPK α subunit in Caenorhabditis elegans, designated aak-2, increases lifespan. Here we show the interaction of aak-2 with other pathways known to control aging in worms. Lifespan extension caused by daf-2/insulin-like signaling mutations was highly dependent on aak-2, as was the lifespan extension caused by over-expression of the deacetylase, sir-2.1. Similarly, there was partial requirement for aak-2 in lifespan extension by mitochondrial mutations (isp-1 and clk-1). Conversely, aak-2 was not required for lifespan extension in mutants lacking germline stem cells (glp-1) or mutants of the eating response (eat-2). These results show that aging is controlled by overlapping but distinct pathways and that AMPK/aak-2 represents a node in a network of evolutionarily conserved biochemical pathways that control aging." - Aging Cell Online Early |
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