Sentence examples similar to activate aging from inspiring English sources

While amino acids and carbohydrates can directly activate aging-pathways such as mTOR and insulin/IGF-1, the role of specific proteins targeted by fatty acids and their potential role in aging is still unclear (Hou & Taubert, 2012; Hansen et al., 2013).

AGE precursors such as methylglyoxal (MG) also activate AGE receptors, with an in vivo study demonstrating endogenous MG synthesis increased in parallel with hyperglycemia [ 34].

Given that IKK-beta is activated in aging hypothalamus, one may suggest that MTOR is activated too.

The progerin mutation is de novo activated during aging [ 5], and its expression is increased during in vitro propagation [ 16].

The same hypothalamic inflammatory pathway is activated during aging while direct blockade of hypothalamic inflammation slows down aging in rodents [ 3].

In somatic cells the p53/p21 pathway is progressively activated during aging as telomeres are lost and cells accumulate DNA damage, eventually promoting senescence [ 61].

In this context, p21RAS, MEK, and MAPkinases activating NF-kappaB were shown to interact with RAGE [ 18], however it is unknown whether they are activated in aging and RDEB.

High-power images revealed that Iba1-IR cells in 10-week-old mice were characterized by a small soma and numerous thin, branched processes (ramified), whereas those in 90-week-old mice had a larger soma with fewer and shorter processes in both WT and KO mice, suggesting that microglia were activated with aging.

When ligand-bound, DAF-2 triggers the IIS pathway [ 77] by activating AGE-1, a homolog of p11, the catalytic subunit of human phosphatidylinositol 3-kinase (PI3K) [ 6]. (Of note: allelic variation in PI3K appears to affect human longevity, as determined by comparing the representation of genotypes in younger and older age groups [ 76, 78]).

The age-1 dependent DAF-16 translocation we have discovered also suggests that long-term starvation activates AGE-1, which is a surprising conclusion considering current models proposing that Class IA PI3Ks are downstream targets of insulin-induced signalling in response to feeding.

We also looked at PERK and eIF2α activation in young controls to determine if ER stress is activated in normal aging.