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.
By inhibiting the activation of NF-κB, HIV-1 Vpu exerts much broader immunosuppressive effects than previously anticipated and may be an important determinant of chronic inflammation in HIV-1 infected individuals.
Building on previous work (Fu et al., 2016), we demonstrate the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB signaling in the colon and the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival/recovery from extrinsic DNA damage.
A long non-coding RNA removes the transcriptional repressor p50 to regulate recruitment of co-activator p300 and RNA Polymerase II complexes to activate the COX-2 gene in human mammary epithelial cells and macrophages.
TRAF3, a negative regulator of noncanonical NF-κB signaling, maintains epithelial cell quiescence at confluence, and its loss triggers upregulation of immunity genes and prevents entry into G0 at high cell density.
The thioredoxin-1 (Trx1) system promotes inflammation by positively regulating both NLRP3 inflammasome responses, by detoxifying excessive ROS independently of Txnip and NF-κB binding to target DNA.
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.
The integration of signals via the pleiotropic NF-kappaB (NF-κB) system enables microenvironmental cues to tune cellular responses to pathogenic substances.
