Related Experiment Video
Updated: Feb 24, 2026

A Macrophage Reporter Cell Assay to Examine Toll-Like Receptor-Mediated NF-kB/AP-1 Signaling on Adsorbed Protein Layers on Polymeric Surfaces
Published on: January 7, 2020
RGS10 differentially modulates NFKB subunit transcription and inflammatory cytokine profiles in peritoneal
Janna E Jernigan Posey1,2,3,4, Kruthika Dheeravath1,2,3, Cassandra L Cole1,2,3,4
1Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, FL, USA.
None:
Regulator of G-protein signaling 10 (RGS10) has been shown to regulate multiple inflammatory pathways relevant to disease pathogenesis. Of particular importance is the ability of RGS10 to negatively regulate the NFkB pathway, a prominent pro-inflammatory pathway implicated in multiple inflammatory disease phenotypes. However, the exact mechanism by which RGS10 regulates NFkB is unknown. Considering that RGS10 translocates into the nucleus upon stimulation, we hypothesize that RGS10 may regulate NFKB through transcription. To determine whether RGS10 mediates NFkB transcription, we stimulated RGS10 KO and B6 peritoneal macrophages and collected cell lysate over 24 hours to assess transcript levels of NFkB and related proinflammatory cytokines. Here we found that RGS10 differentially regulates the transcription of NκKB subunits and NFκB-dependent cytokines. Further studies are warranted to understand the potential role of RGS10 in transcriptional regulation of inflammatory states.
More Related Videos
10:21Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
10:35Assessment of Antibody-based Drugs Effects on Murine Bone Marrow and Peritoneal Macrophage Activation
Published on: December 26, 2017