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Titlebook: Sirtuins; Riekelt H. Houtkooper Book 2016 Springer Science+Business Media Dordrecht 2016 Sirtuin.Aging.Metabolic Disease.Nicotinamide Aden

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21#
發(fā)表于 2025-3-25 03:45:38 | 只看該作者
SIRT1 in Metabolic Health and Disease,s rapidly envisioned. More than a decade later, SIRT1 has been demonstrated to be at the pinnacle of metabolic control and metabolic adaptation in diverse organisms, including mammals. The activation of SIRT1 has been shown to be protective against metabolic damage and also holds promise in the batt
22#
發(fā)表于 2025-3-25 09:08:44 | 只看該作者
Deacetylation by SIRT3 Relieves Inhibition of Mitochondrial Protein Function,n acetylation is regulated by the sirtuin SIRT3, which has been reported to control several metabolic pathways. While the functional relevance of protein acetylation is likely specific for proteins in different pathways, a picture is emerging for mitochondrial protein acetylation to be an important
23#
發(fā)表于 2025-3-25 14:28:18 | 只看該作者
24#
發(fā)表于 2025-3-25 17:51:14 | 只看該作者
25#
發(fā)表于 2025-3-25 22:11:12 | 只看該作者
26#
發(fā)表于 2025-3-26 03:02:59 | 只看該作者
27#
發(fā)表于 2025-3-26 05:14:38 | 只看該作者
Sirtuins and Aging,a molecular level, these diseases are associated with a plethora of pathophysiological mechanisms, including deficiency in nutrient sensing, proteostasis, and mitochondrial function. Sirtuins have been implicated in the age-related malfunctioning of these pathways and are thought to be involved in t
28#
發(fā)表于 2025-3-26 08:58:22 | 只看該作者
Sirtuins and the Circadian Clock: Epigenetic and Metabolic Crosstalk,lso deacetylates specific elements of the clock machinery and modifies histones to regulate gene expression. In this chapter, we review the current understanding of the field on the interrelationship between SIRT1 and the circadian clock machinery, how this regulation occurs, and what other possible
29#
發(fā)表于 2025-3-26 13:35:18 | 只看該作者
30#
發(fā)表于 2025-3-26 19:24:36 | 只看該作者
Sirtuins: A Future Perspective, as well as chronic disease states and metabolism. Interventions targeting human aging and disease are in or on their way to the clinic. Perhaps the most surprising aspect of this is that it all started with yeast aging. Where will it end? One thing seems clear. Our knowledge of mammalian biology ha
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