A novel master regulatory mechanism of cell proliferation and senscence employs the lncRNA UCA1 and a CAPERα/TBX3 corepressor.

The PBAF chromatin-remodelling complex is essential for the proliferation of melanocytes and melanoma cells and is recruited to critical regulatory elements by physical and functional interactions with MITF, a transcription factor and master regulator of melanoma.

Senescent cells are recurrently induced during limb regeneration in salamanders and subsequently eliminated by a highly efficient mechanism of macrophage-dependent surveillance.

The ATM kinase has an unanticipated role in tumor progression through the regulation of cell migration by oxidative stress.

Senescent cells contribute to age-related fat dysfunction and can directly impair healthy fat progenitor function, in part, via the secretion of activin A.

Inflammatory cells differentially regulate a scarring versus a regenerating response to injury in mammals.

While acute senescence of decidualizing cells drives the inflammatory response underpinning uterine receptivity, subsequent clearance by activated natural killer cells transiently rejuvenates the cycling endometrium, enabling transition into a gestational tissue upon embryo implantation.

A genetic screen in combination with biochemical approaches reveal hijacking of the host β-catenin destruction complex by the parasite T. gondii to reprogram immune gene expression.

miR-34a prevents inflammation-induced colonic regeneration from oncogenesis by simultaneously targeting processes in both immune and epithelial cells, including T helper 17 cell differentiation, recruitment, and IL-17 induced epithelial proliferation.

Tissue damage induces a reversible cell cycle arrest in G2, which promotes survival and mitogenic signals to facilitate tissue regeneration but drives senescence-like phenotypes under chronic stress conditions.