Andria Rasile Robinson

TL;DR: It is concluded that unrepaired cytotoxic DNA damage induces a highly conserved metabolic response mediated by the IGF1/insulin pathway, which re-allocates resources from growth to somatic preservation and life extension, and demonstrates that ageing and end-of-life fitness are determined both by stochastic damage and genetics.

TL;DR: Results indicate that the mechanism by which DNA damage drives aging is due in part to NF-κB activation and IKK/NF-κBs inhibitors are sufficient to attenuate this damage and could provide clinical benefit for degenerative changes associated with accelerated aging disorders and normal aging.

TL;DR: Data support the conclusion that, as in yeast, ERCC1-XPF facilitates DSB repair via an end-joining mechanism that is Ku86 independent, and in vitro repair of DSBs with 3′ overhangs led to large deletions in the absence of ERCC 1- XPF.

TL;DR: Endocrine and metabolic changes are indicative of “survival” responses to genotoxic stress or starvation, whereas genome-wide associations in gene expression with natural aging are indication of biological age, which may delineate pro- and anti-aging effects of treatments aimed at health-span extension.

TL;DR: The clinical severity, coupled with a relatively mild repair defect, suggests novel functions for ERCC1, and represents a novel complementation group of patients with defective NER.