When exposed to high-dose ionizing radiation, tardigrades undergo extensive DNA damage, like humans, but cope by stimulating expression of DNA repair proteins and of TDR1, a novel tardigrade-specific DNA-binding protein.

Experiments on E. coli show that multiple mechanisms contribute to extreme resistance to ionizing radiation in bacteria, with mutations to three genes for DNA repair having a prominent role in one evolved population.

Tiny animals known as tardigrades use a combination of DNA repair machinery and a novel protein to mend their genome after intense ionizing radiation.

Loss of foxo rescues age-related defects in stem cell-mediated regeneration post-injury.

Dsup, a unique protein found only in tardigrades, is a nucleosome-binding protein that protects DNA from damage by hydroxyl radicals, such as those generated by ionizing radiation or oxidants.

Drosophila p53 protein isoforms function during oogenesis to ensure the integrity of the transmitted genome, a function that is conserved to humans.

Subterranean isopods endemic to regions with large igneous rock formations have a higher mutation rate and display an excess of mutations that are typical of an oxidative stress.

Irradiation of normal human fibroblasts and mice in conditions mimicking standard external X-ray radiotherapy protocols highlights that noncancerous cells surrounding the planning target volume accumulate DNA single-strand breaks but almost no double-strand breaks, putting them in a pre-cancerous senescent state.

Estrogen is a systemic factor that promotes hematopoietic regeneration by activating the unfolded protein responses.