Activated macrophages initiate a robust DNA damage response that depends on type I IFN and regulates their genetic program and inflammasome activation, establishing a mechanistic link between DNA damage responses and innate immunity.

Experimental manipulation of a core DNA damage response factor and cell-cycle checkpoint regulators reveals a key role for these processes in the progenitor cells that fuel limb regeneration.

Cell cycle arrest in response to a double-stranded break is initially maintained by the DNA damage checkpoint and later by the spindle assembly checkpoint.

Disruption of TFEB and TFE3 results in diminished p53 signaling capacity and altered cell cycle regulation under genotoxic stress conditions.

Phase separated DNA-free stored forms of RecA dissolve in response to DNA damage to make RecA available for repair and recombination reactions as part of the bacterial (Escherichia coli) SOS response.

Unbiased analyses highlight context-specific crosstalk between Notch, DNA damage response genes, and PP2A, and provide a roadmap for understanding how Notch induces squamous cell differentiation.

The dual function of an ancient prokaryotic enzyme, which is linked to specific metabolite signals, may have been the evolutionary driving force behind its dual localization in eukaryotes.

SIRT1 deacetylates SIRT6 at K33 to facilitate DNA double-strand breaks-recognition, subsequent expansion and local chromatin remodeling.

Structural characterization of human RPA70N association with a series of DNA damage response proteins reveals versatile protein interaction mechanisms that help to recruit DNA repair proteins to the damage site quickly and efficiently.

Banp is a transcription activator of cell cycle genes like cenpt, ncapg, and wrnip1 to prevent genotoxic stress during rapid cell division and its repercussions on development and disease.