Journal ArticleDOI
Regulation of Aging and Age-Related Disease by DAF-16 and Heat-Shock Factor
TLDR
The findings suggest that HSF-1 and DAF-16 together activate expression of specific genes, including genes encoding small heat-shock proteins, which in turn promote longevity, which couple the normal aging process to this type of age-related disease.Citations
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疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Journal ArticleDOI
The Hallmarks of Aging
TL;DR: Nine tentative hallmarks that represent common denominators of aging in different organisms are enumerated, with special emphasis on mammalian aging, to identify pharmaceutical targets to improve human health during aging, with minimal side effects.
Journal ArticleDOI
Adapting proteostasis for disease intervention.
TL;DR: The proteostasis network is described, a set of interacting activities that maintain the health of proteome and the organism that has the potential to ameliorate some of the most challenging diseases of this era.
Journal ArticleDOI
The plasticity of aging: insights from long-lived mutants.
TL;DR: Mutations in genes affecting endocrine signaling, stress responses, metabolism, and telomeres can all increase the life spans of model organisms, leading to a mechanistic understanding of how these two processes--aging and disease susceptibility--are linked.
Journal ArticleDOI
Heat shock factors: integrators of cell stress, development and lifespan
TL;DR: These unexpected observations have uncovered complex layers of post-translational regulation of HSFs that integrate the metabolic state of the cell with stress biology, and in doing so control fundamental aspects of the health of the proteome and ageing.
References
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疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A
TL;DR: PfPMP1）与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作�ly.
Journal ArticleDOI
A C. elegans mutant that lives twice as long as wild type
TL;DR: Finding that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild type raises the possibility that the longevity of the dauer is not simply a consequence of its arrested growth, but instead results from a regulated lifespan extension mechanism that can be uncoupled from other aspects of dauer formation.
Journal ArticleDOI
Alpha-crystallin can function as a molecular chaperone
TL;DR: It is shown that alpha-crystallin refracts light and protects proteins from aggregation in the transparent eye lens and that in nonlens cells alpha-Crystallin may have other functions in addition to its capacity to suppress aggregation of proteins.
Journal ArticleDOI
Genetic pathways that regulate ageing in model organisms
Leonard Guarente,Cynthia Kenyon +1 more
TL;DR: Genetic studies in genetically tractable model organisms established that ageing is indeed regulated by specific genes, and allowed an analysis of the pathways involved, linking physiology, signal transduction and gene regulation.
Journal ArticleDOI
Regulation of the Caenorhabditis elegans longevity protein DAF-16 by insulin/IGF-1 and germline signaling.
TL;DR: It is shown that the D AF-2 pathway prevents DAF-16 accumulation in nuclei, and it is found that both sensory neurons and germline activity regulate DAF/IGF-1 signaling, but the nuclear localization patterns are different, which reveal unexpected complexity in the Daf-16-dependent pathways that regulate aging.