Genetic analysis of tissue aging in Caenorhabditis elegans: a role for heat-shock factor and bacterial proliferation.
By D. Garigan, A. Hsu, Andrew G. Fraser, R. Kamath, J. Ahringer, C. Kenyon. Genetics, 2002
854 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/9167df4d8e5bf0f76edcf38cdd8a337de272b808
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- C. Kenyon
- Rute Martins
- Richard I. Morimoto
- Nataliya Libina
- Anat Ben-Zvi
- Javier Apfeld
- E. Troemel
- G. Lithgow
Citations in the corpus
- Widespread Protein Aggregation as an Inherent Part of Aging in C. elegans (2010, background): “As the integrity of muscle tissue degenerates sharply with age [51,52], intracellular localization of age-dependent aggregates becomes challenging.”
- The AMP-activated protein kinase AAK-2 links energy levels and insulin-like signals to lifespan in C. elegans. (2004, background): “Moreover, a lipofuscin-like fluorescent pigment that accumulates in an age-dependent manner in the intestine (Garigan et al. 2002; Herndon et al. 2002) accumulates at a faster rate in aak-2 mutants than in wild-type animals (Fig.”
- Genes that act downstream of DAF-16 to influence the lifespan of Caenorhabditis elegans (2003, background): “The early ageing transcriptome is largely unaffected Because mutations in the insulin/IGF-I pathway slow the rate of agein”
- The genetics of ageing (2010, background): “The most remarkable thing about these (and many other) long-lived mutants is that they remain young long after normal worms look ol”
- SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response. (2003, background): “elegans, aging involves pleiotropic changes that vary among individuals, and mutations that influence lifespan may affect aging of some tissues more than others (Garigan et al. 2002; Herndon et al. 2002).”
- Metformin Retards Aging in C. elegans by Altering Microbial Folate and Methionine Metabolism (2013, background): “In senescent worms, E. coli contribute to the demise of their host, clogging the lumen of the alimentary canal and invading the intestine (Garigan et al., 2002; Labrousse et al., 2000; McGee et al., 2011).”
- p38 MAPK Regulates Expression of Immune Response Genes and Contributes to Longevity in C. elegans (2006, background): “coli, their normal laboratory food source, and nematodes live longer on killed bacteria than on live bacteria [24,25].”
- Sirtuins in aging and age-related disease. (2006, background): “elegans, where it was shown that reduced insulin/IGF-1 signaling can slow a variety of age-related phenotypes in distinct tissues (Garigan et al., 2002).”
- FOXO/4E-BP Signaling in Drosophila Muscles Regulates Organism-wide Proteostasis During Aging (2010, background): “In addition, because most tissues undergo progressive deterioration during aging (Garigan et al., 2002), it is thought that organismal life span may be linked to tissue senescence.”
- The plasticity of aging: insights from long-lived mutants. (2005, background): “The antibacterial genes are also interesting since bacterial proliferation contributes to the death of C. elegans (Garigan et al., 2002; Gems and Riddle, 2000) and daf-2 mutants are resistant to pathogens (Garsin et al., 2003).”
- Long live FOXO: unraveling the role of FOXO proteins in aging and longevity (2015, background): “HSF-1, along with DAF-16, promotes longevity by activating specific longevity genes, including genes that encode small heat-shock proteins (Garigan et al., 2002; Hsu et al., 2003; Walker & Lithgow, 2003; Morley & Morimoto, 2004).”
- Tissue-specific activities of C. elegans DAF-16 in the regulation of lifespan. (2003, background): “…a single animal, the rates of decline of different tissuescurious that lifespan could be extended without the inappear to be similar to one another (Garigan et al., 2002).creased expression of the stress-response gene sod-3 Thus, epigenetic mechanisms must play an importantin every tissue (see…”
- Collapse of proteostasis represents an early molecular event in Caenorhabditis elegans aging (2009, methodology): “Animals were stained with rhodamine phalloidin (Molecular Probes) and with either anti-paramyosin [5-23] (57), anti-myosin heavy chain B [28.”
- Regulation of longevity in Caenorhabditis elegans by heat shock factor and molecular chaperones. (2003, background): “These results corroborate previous observations that HSF-1 levels influence the rate of aging (Garigan et al., 2002) and that hsf-1(RNAi) inhibits daf-2 mediated longevity (Hsu et al.”
- Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans (2002, background): “) might normally influence the rate of ageing in several tissue”