To promote longevity under heat stress shares yeast aging factors with progeny through a down-regulation of the diffusion barrier in the membranes between the mitotic cells.

Epigenetic drift of H3K27me3 is one of the molecular mechanisms that contribute to aging, and stimulation of glycolysis promotes metabolic health and longevity.

Cell biological and genetic studies reveal age-associated alterations of lysosomes and modulation of lysosomal activity by longevity pathways.

Translational evidence indicates APOE2 benefits longevity independent of its protective effects on Alzheimer’s disease, which preserved activity and the metabolism of apoE protein and associated-lipids would be key to understanding.

Extensive molecular profiling shows how loss of highly similar, paralogous ribosomal proteins lead to distinct phenotypic outputs, through translational control of specific mRNAs.

Endo-siRNAs slow down the rate of aging and enable the maintenance of a responsive heat shock response in aging germline-less Caenorhabditis elegans.

Two SET-domain containing proteins regulate H3K4me3 by their binding to H3K4me3 through their PHD domain and directly regulate expression of a subset of genes.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

Modulating the nutrient sensor TORC1 only in neurons in C. elegans is sufficient to regulate systemic longevity via inter-tissue signals that remodel mitochondria networks in non neuronal cells.

A mouse model reveals that a p53 SNP impacts longevity via modulating the balance of cancer risk and the self-renewal function of stem/progenitor cells, which supports a role of p53 in regulation of longevity.