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.
The integration of signals via the pleiotropic NF-kappaB (NF-κB) system enables microenvironmental cues to tune cellular responses to pathogenic substances.
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.
Cell imaging and mathematical modelling show reciprocal cross-regulation between inflammatory signalling and cell cycle timing, which is mediated through functional interactions between NF-B and E2F proteins.
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.
Circulating human primed innate lymphoid cell precursors have the potential to functionally induce adhesion molecules' expression in endothelial cells and possibly support the immune cells' infiltration into the tumor site.
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.
