The Cdkn1a gene (p21Waf1/Cip1) is an inflammatory response gene in the mouse central nervous system

Absence of the cell cycle inhibitor p21Cip1 reduces LPS‐induced NO release and activation of the transcription factor NF‐κB in mixed glial cultures

“…In other words, p21 Cip1 facilitates, rather than inhibits, LPS-induced NO release and NF-B activation while inhibiting LPS-induced TNF-␣ release. The results presented here are in agreement with those obtained by Ring et al (2003) in an in vivo study using LPS administration as a model for sepsis and acute inflammation. These investigators reported that cdkn1a gene (p21 Cip1 ) is induced in the mouse CNS as part of the acute response to inflammation, suggesting that the induction is most likely to be a downstream event of cytokine signaling involving the toll-like receptor 4 (TLR4).…”

DNA Repair and Cell Cycle Biomarkers of Radiation Exposure and Inflammation Stress in Human Blood

“…Our finding seriously undermines the promise of CDKN1A as a predictive tool for radiation exposure in individuals suffering simultaneous inflammatory stress. Studies in the murine central nervous system also identified CDKN1A as an inflammatory response gene [44] and LPS exposure upregulated CDKN1A transcripts in mice [30]. LPS-induced and the radiation-induced CDKN1A responses were indistinguishable in our human blood model, while in the mouse the upregulation of CDKN1A at 24 hours after LPS injection did not mask the ability to detect a radiation response [30].…”

Chromatin Remodeling Factor Brg1 Supports the Early Maintenance and Late Responsiveness of Nestin-Lineage Adult Neural Stem and Progenitor Cells

“…It is also possible that p53 protein is stabilized following Brg1 deletion , or there exists p53 post‐transcriptional regulatory mechanisms . Given the challenges of visualizing increases in p53+ or p21+ cells in the healthy adult mouse hippocampus , this hypothesis is ripe for testing using other approaches, such as cell cycle reporter mice .…”