Oncoprotein BCL6 confers tumor adaptive resistance to genotoxic stress through the IFN-BCL6-PTEN axis in solid tumors and presents a promising combinational target for chemo-sensitization.

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.

The nuclear protein Sam68 plays a role in the genotoxic stress-initiated "nuclear to cytoplasmic" activation of NF-κB and is involved in the development and survival of colon cancer.

Minimizing anti-proliferation signaling from DNA damage detection machinery is the tactic for the cells to drive proliferation under genotoxic environment, and the function is exerted by Polo-Like-Kinase1 that is frequently over-expressed in cancer cells.

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

The interaction of ImuB with the β sliding clamp is essential for induced mutagenesis in mycobacteria and could be a novel target for new anti-tuberculosis drugs designed to inhibit the emergence of genetic resistance.

In vivo single-molecule imaging demonstrates that Smc5/6 chromatin association depends on ATP hydrolysis and dsDNA binding, requires Nse6 and is modulated by Brc1 after DNA damage.

Leukemia-Related Protein 16 (LRP16), a member of the macro domain family, plays a crucial role in orchestrating genotoxicity-initiated NF-κB signaling in the colon and the pathophysiological relevance of NF-κB activation induced by LRP16 in colonic cell survival/recovery from extrinsic DNA damage.

Wss1 is both a metalloprotease and SUMO ligase found in association with Cdc48 and Doa1 and accumulating in the vacuole upon DNA damage.

Upon genotoxic stress, the FBXL10-RNF68-RNF2 ubiquitin ligase complex mono-ubiquitylates histone H2A and mediates H2A/H2A.Z exchange to repress transcription and ensures proper high fidelity homologous recombination repair.