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.

The neutral amino acid transporter SLC38A2 is an essential protective factor for renal medulla during urine concentration.

A live imaging and computational approach reveals feedback loops involving F-actin dynamics that regulate the NF-κB transcription factor RELA.

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

IL-33 plays an important role in the initiation of labor by leading to stress of the ER via an influx of calcium ions in human uterine smooth muscle cells.

The mechanistic characterization of NF-κB transcription inhibition by anthracyclines opens new possibilities for improved cancer chemotherapy and the treatment of inflammation-driven conditions.

A long non-coding RNA regulates the expression of genes that encode proteins involved in the inflammatory response.

Chronic and excessive inflammation can lead to exhaustion of the supply of hematopoietic stem cells and to myeloid malignancies in mice, mimicking important aspects of the myelodysplastic syndrome found in humans.

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.

A model of early postnatal bacterial meningitis in the mouse demonstrates the transcriptome responses of each of the major meningeal cell types and should prove useful in dissecting the pathophysiology of bacterial meningitis in human infants.