An atmospheric trigger, the respirable particulate matter boost microglia pathogenic activities in the context of CNS demyelination by activating TLR-4/NF-kB signaling axis in animal models of immune- and toxicity-induced demyelination, as well as myelinogenesis during postnatal development.

Structural and biophysical characterization of NF-κB p52 in complex with closely related DNAs reveals the dynamic states of central base pair(s) have a strong influence on transcriptional activity of p52.

During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

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

Site-specific modification of NEMO facilitates RANKL signal specificity in myeloid progenitors and serves as a potential target to modulate inflammatory osteolysis through ISG15-dependent autophagy.

Genetic mouse models show that hepatic NIK and IKKα inhibit hepatocyte proliferation and liver regeneration in part by inhibiting the JAK2/STAT3 pathway.

Intrinsic defects in keratinocytes can cause skin inflammation through excessive cell death and production of inflammatory molecules.

Retention of Caspase-8 confers a selective advantage to glioblastoma and represents a novel therapeutic target.

Detailed biochemical and metabolic analysis of the inflammatory response in human endothelial cells reveals that inflammation directly regulates cholesterol homeostasis.