DAF-16 Target Genes That Control C. elegans Life-Span and Metabolism

By Siu Sylvia Lee, Scott Kennedy, Andrew C. Tolonen, Gary Ruvkun. Science, 2003

723 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c46f541b4620fe6f77059e7b22981b016311d678

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Citations in the corpus

FoxOs are critical mediators of hematopoietic stem cell resistance to physiologic oxidative stress. (2007, background): “…the oxidative stress response is regulated in part by FoxO induction of MnSOD, catalase, and GADD45 (Kops et al., 2002a; Nemoto and Finkel, 2002; Tran et al., 2002), and has been linked to longevity and dauer formation in C. elegans (Honda and Honda, 1999; Lee et al., 2003; Murphy et al., 2003).”
Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans (2003, background): “Note added in proof: While this paper was in review, two independent studies of genes regulated by daf-16 were publishe”
A Role for Autophagy in the Extension of Lifespan by Dietary Restriction in C. elegans (2008, background): “16 antimicrobial, metabolic and other genes that act in a cumulative fashion to extend lifespan [54-57].”
A Mitochondrial Paradigm of Metabolic and Degenerative Diseases, Aging, and Cancer: A Dawn for Evolutionary Medicine (2005, background): “elegans genome have been proposed to have a mitochondrial function, mitochondrial functions must have a much greater influence on longevity than other physiological processes (109, 110).”
FoxOs at the crossroads of cellular metabolism, differentiation, and transformation. (2004, neutral): “2, 20.as those identified through genetic screens for Daf16 Kau, T.R., Schroeder, F., Ramaswamy, S., Wojciechowski, C.L.,targets in C. elegans (Lee et al., 2003; Murphy et al., Zhao, J.J., Roberts, T.M., Clardy, J., Sellers, W.R., and Silver, P.A. 2003).”
Nonequilibrium physics in biology (2019, result): “Further analysis of the ageing and rejuvenation attractors suggests that self-degradation of lifespan-limiting and longevity-promoting genes leads to an increased stability of the ageing and rejuvenation states, respectively, which is consistent with experiments (Apfeld et al., 2004; Kenyon et al., ”
Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans (2010, background): “Inherent Protein Aggregation Is Modulated by the Insulin/IGF-1 Signaling Pathway Reducing insulin/IGF-1 signaling is known to trigger the expression of many cell-protective proteins and processes [69,70,71,72] that prevent the collapse of proteostasis.”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “16/FoxO as a central player of a complex network involving multiple upstream pathways and downstream target genes (Lee et al., 2003; McElwee et al., 2003; Murphy et al., 2003).”
TOR signaling and rapamycin influence longevity by regulating SKN-1/Nrf and DAF-16/FoxO (2012, background): “IIS, TORC1, and TORC2 are each involved in growth, and SKN-1 and DAF-16 functions include maintenance of protein homeostasis and resistance to various stresses (Kenyon , 2010; Lee et al., 2003; Li et al., 2011; McElwee et al., 2007; Murphy et al., 2003; Oliveira et al., 2009).”
Tissue-specific activities of C. elegans DAF-16 in the regulation of lifespan. (2003, background): “We of lipophilic hormones, are regulated in a daf-16-depen-suggest that this network of tissue interactions and dent manner (Lee et al., 2003; McElwee et al., 2003;feedback regulation allows the tissues to equilibrate Murakami and Johnson, 2001; Murphy et al., 2003).and fine-tune their expression…”
The TOR pathway interacts with the insulin signaling pathway to regulate C. elegans larval development, metabolism and life span (2004, background): “…DAF-2/insulin and CeTOR signaling pathways In ulin signaling can modulate the TOR pathway in mammals (Schmelzle and Hall, 2000), and in C. elegans the DAF-2 insulin/IGF pathway functions to inhibit its major target, DAF16, a FOXO family transcription factor (Lin et al., 1997; Ogg et al., 1997).”
A conserved MST-FOXO signaling pathway mediates oxidative-stress responses and extends life span. (2006, positive): “Consistent with these results, antioxidant and other stress-response genes constitute a prominent set of DAF-16-regulated genes (Lee et al., 2003a; McElwee et al., 2004; Murphy et al., 2003).”