Tissue-specific activities of C. elegans DAF-16 in the regulation of lifespan.

By Nataliya Libina, Jennifer R. Berman, C. Kenyon. Cell, 2003

798 citations recorded by the source corpus.

Subfields: Aging, Endocrine and Autonomic Systems, Rheumatology

View Paper: https://www.semanticscholar.org/paper/b6dacb973d2fd9653bb3ccab1a3c1501ee023ad2

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Citations in the corpus

SIRT2 deacetylates FOXO3a in response to oxidative stress and caloric restriction (2007, background): “Increasing daf-16 activity in the intestine of worms delays aging (Libina et al ., 2003).”
A conserved MST-FOXO signaling pathway mediates oxidative-stress responses and extends life span. (2006, positive): “Recent studies also point to several circumstances that uncouple life-span extension from resistance to stress signals (Lee et al., 2003b; Libina et al., 2003).”
FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, background): “Manipulation of longevity-regulating pathways in certain tissues is sufficient to extend life expectancy, indicating that some tissues have a predominant role in life span extension (Libina et al., 2003; Wang et al., 2005; Wolkow et al., 2000).”
The Cell Non-Autonomous Nature of Electron Transport Chain-Mediated Longevity (2011, positive): “…or reduction of insulin/IGF-1 signaling (IIS) in neuronal or fat tissues (Broughton et al., 2005; Hwangbo et al., 2004; Kapahi et al., 2004; Libina et al., 2003; Wolkow et al., 2000); and genetic manipulations to specific neurons which then alter the capacity for the entire animal to…”
p38 MAPK Regulates Expression of Immune Response Genes and Contributes to Longevity in C. elegans (2006, methodology): “We tested three genes: mtl-1, because this gene had the greatest fold change; sod-3, because it is a commonly used marker for DAF-16 activity [26]; and lys-7,”
The C. elegans TGF-β Dauer Pathway Regulates Longevity via Insulin Signaling (2007, positive): “sod-3 (superoxide dismutase) is a direct transcriptional target of DAF-16 [21, 22], and the expression of a Psod-3::gfp reporter is increased broadly in daf-2 mutants [23].”
Regulation of lifespan in Drosophila by modulation of genes in the TOR signaling pathway. (2004, neutral): “elegans nervous system has been shown to be sufficient for lifespan extension [40,41].”
Metformin Induces a Dietary Restriction–Like State and the Oxidative Stress Response to Extend C. elegans Healthspan via AMPK, LKB1, and SKN-1 (2010, background): “To determine whether SKN-1 acts in either the ASI neurons or the intestine to mediate metformin-induced healthspan extension, we tested genetic mosaics that express tissue-appropriate isoforms of skn-1 from the gpa-4 promoter specific to ASI neurons [74] or the ges-1 promoter specific to the intesti”
The plasticity of aging: insights from long-lived mutants. (2005, background): “Removing the germ cells causes DAF-16 nuclear localization primarily in the intestine/adipose tissue (Lin et al., 2001), and its activity there is sufficient to account for the entire life span extension produced by removal of the germline (Libina et al., 2003).”
Neural mechanisms of ageing and cognitive decline (2010, background): “In worms, for example, reduced IIS in the nervous system accounts for a portion of the lifespan extension in IIS mutant”
Compartment-specific perturbation of protein handling activates genes encoding mitochondrial chaperones (2004, methodology): “…signal peptide (Labrousse et al., 1999) was gift from Alexander van der Bliek (University of California Los Angeles, USA) and the strain expressing sod-3::gfp (muIs84, CF1553) (Libina et al., 2003) was a gift from Malene Hansen and Cynthia Kenyon (University of California San Francisco, USA).”
Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “specifically in one tissue (intestine/adipose tissue) can increase the worm lifespan by 60% (Libina et al., 2003).”