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RT СµÜ²ËÄñ,½ñÌì²éÎÄÏ×ÕÒµ½Ò»¸ö"doi:10.1016/j.bbagen.2009.06.007",ÇëÎʸ÷λ,ÈçºÎÕÒµ½È«ÎÄÁ´½ÓÄØ? |
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taochn
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jhliu001(½ð±Ò+5,VIP+0):½â¾öÁËÒ»Ö±À§ÈÅÎÒµÄÎÊÌâ,¶àл! 7-9 09:32
jhliu001(½ð±Ò+5,VIP+0):½â¾öÁËÒ»Ö±À§ÈÅÎÒµÄÎÊÌâ,¶àл! 7-9 09:32
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ʹÓÃËÑË÷ÒýÇæ£º http://dx.doi.org/ Review The TOR pathway comes of age Monique N. Stanfela, Lara S. Shamiehb, Matt Kaeberleinb, and Brian K. Kennedya, , aDepartment of Biochemistry, University of Washington, Seattle, WA 98195, USA bDepartment of Pathology, University of Washington, Seattle, WA 98195, USA Received 23 February 2009; revised 10 June 2009; accepted 11 June 2009. Available online 16 June 2009. Abstract Studies in a variety of model organisms indicate that nutrient signaling is tightly coupled to longevity. In nutrient replete conditions, organisms develop, grow, and age quickly. When nutrients become sparse as with dietary restriction, growth and development decline, stress response pathways become induced and organisms live longer. Considerable effort has been devoted to understanding the molecular events mediating lifespan extension by dietary restriction. One central focus has been on nutrient-responsive signal transduction pathways including insulin/IGF-1, AMP kinase, protein kinase A and the TOR pathway. Here we describe the increasingly prominent links between TOR signaling and aging in invertebrates. Longevity studies in mammals are not published to date. Instead, we highlight studies in mouse models, which indicate that dampening the TOR pathway leads to widespread protection from an array of age-related diseases. Keywords: Aging; TOR; S6 kinase; Neurodegeneration; Metabolic syndrome; Cardiovascular disease; Dietary restriction [ Last edited by taochn on 2009-7-9 at 09:28 ] |
2Â¥2009-07-09 09:26:49
springimu
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3Â¥2009-07-09 09:32:29
victory_liu
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4Â¥2009-07-09 09:36:59













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