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.

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.

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.

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.

NF-κB oscillations synchronize to external perturbations as a damped oscillator, producing different transcription dynamics.

The integration of signals via the pleiotropic NF-kappaB (NF-κB) system enables microenvironmental cues to tune cellular responses to pathogenic substances.

The deubiquitinating enzyme YOD1 binds to the E3 ligase TRAF6 to counteract p62/sequestosome1 mediated pro-inflammatory NF-κB signaling in response to interleukin-1.

A novel high-throughput, whole organism chemical screening platform was used to identify existing drugs that increase pancreatic beta-cell mass in zebrafish, implicating unique roles for the NF-κB and serotonergic signaling pathways in regulating pancreatic biology.