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Rifampicin reduces advanced glycation end products and activates DAF‐16 to increase lifespan in Caenorhabditis elegans
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Sandeep Golegaonkar Syed S. Tabrez Awadhesh Pandit Shalini Sethurathinam Mashanipalya G. Jagadeeshaprasad Sneha Bansode Srinivasa‐Gopalan Sampathkumar Mahesh J. Kulkarni Arnab Mukhopadhyay 《Aging cell》2015,14(3):463-473
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The SKN‐1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms
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Jennifer M.A. Tullet James W. Green Catherine Au Alexandre Benedetto Maximillian A. Thompson Emily Clark Ann F. Gilliat Adelaide Young Kathrin Schmeisser David Gems 《Aging cell》2017,16(5):1191-1194
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Interventions that slow aging and prevent chronic disease may come from an understanding of how dietary restriction (DR) increases lifespan. Mechanisms proposed to mediate DR longevity include reduced mTOR signaling, activation of the NAD+‐dependent deacylases known as sirtuins, and increases in NAD+ that derive from higher levels of respiration. Here, we explored these hypotheses in Caenorhabditis elegans using a new liquid feeding protocol. DR lifespan extension depended upon a group of regulators that are involved in stress responses and mTOR signaling, and have been implicated in DR by some other regimens [DAF‐16 (FOXO), SKN‐1 (Nrf1/2/3), PHA‐4 (FOXA), AAK‐2 (AMPK)]. Complete DR lifespan extension required the sirtuin SIR‐2.1 (SIRT1), the involvement of which in DR has been debated. The nicotinamidase PNC‐1, a key NAD+ salvage pathway component, was largely required for DR to increase lifespan but not two healthspan indicators: movement and stress resistance. Independently of pnc‐1, DR increased the proportion of respiration that is coupled to ATP production but, surprisingly, reduced overall oxygen consumption. We conclude that stress response and NAD+‐dependent mechanisms are each critical for DR lifespan extension, although some healthspan benefits do not require NAD+ salvage. Under DR conditions, NAD+‐dependent processes may be supported by a DR‐induced shift toward oxidative metabolism rather than an increase in total respiration. 相似文献
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Sarah K. Casper Scott J. Schoeller Danielle M. Zgoba Andrew J. Phillips Thomas J. Morien Gary R. Chaffee Peter C. Sackett Francis C. Peterson Kirsten Crossgrove Christopher T. Veldkamp 《Proteins》2014,82(12):3490-3496
Brugia malayi is a parasitic nematode that causes lymphatic filariasis in humans. Here the solution structure of the forkhead DNA binding domain of Brugia malayi DAF‐16a, a putative ortholog of Caenorhabditis elegans DAF‐16, is reported. It is believed to be the first structure of a forkhead or winged helix domain from an invertebrate. C. elegans DAF‐16 is involved in the insulin/IGF‐I signaling pathway and helps control metabolism, longevity, and development. Conservation of sequence and structure with human FOXO proteins suggests that B. malayi DAF‐16a is a member of the FOXO family of forkhead proteins. Proteins 2014; 82:3490–3496. © 2014 Wiley Periodicals, Inc. 相似文献
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