Regulation of Inflammation by Ubiquitin Modification of Signaling Components |
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| Launch in standalone player | |
| Air date: | Wednesday, May 21, 2008, 3:00:00 PM |
| Category: | Wednesday Afternoon Lectures |
| Runtime: | 75 minutes |
| NLM Title: | Regulation of inflammation by ubiquitin modification of signaling components [electronic resource] / Vishva Dixit. |
| Series: | Ubiquitin modification & inflammasome function in innate immunity |
| Author: | Dixit, Vishva. National Institutes of Health (U.S.) |
| Publisher: | [Bethesda, Md. : National Institutes of Health, 2008] |
| Other Title(s): | Ubiquitin modification & inflammasome function in innate immunity |
| Abstract: | Proper regulation of inflammation is essential for combating pathogen invasion and maintaining homeostasis. Whereas hypo-responsive hosts succumb to infections, unchecked inflammatory reactions promote a variety of debilitating and fatal conditions including septic shock, autoimmune disease, atherosclerosis, graft rejection, and cancer. Pathogens, host immune cell ligands, and pro-inflammatory cytokines such as Tumor Necrosis Factor-a (TNF-a), Interleukin-1-b (IL1-b), and Lipopolysaccharide (LPS) induce an array of inflammatory responses by activating a variety of cell types. Although much is known about how inflammatory responses are initiated and sustained, less is known about how inflammation is attenuated to maintain a homeostatic balance. The A20 protein is now recognized as a central, negative feedback inhibitor, of NF-kB mediated inflammatory responses. It was originally discovered as an NF-kB inducible gene that was recruited to the assembled proximal signaling complex of pro-inflammatory receptors by virtue of being able to bind to other proximal signaling adaptors including TRAFs and RIP. Analysis revealed seven repeats of a novel type of Cys2/Cys2 zinc finger motif at the carboxy terminus that possessed E3 ligase activity and a amino terminal Ovarian Tumor (OTU) domain that exhibited deubiquitinating activity. Both enzymatic activities were shown to act in concert to attenuate NF-kB signaling from pro-inflammatory receptors. |
| Subjects: | Immunity, Innate--physiology Inflammation--metabolism NF-kappa B--metabolism Signal Transduction--physiology Ubiquitination |
| Publication Types: | Government Publications Lectures |
| Download: | Download
Video How to download a Videocast |
| NLM Classification: | QZ 150 |
| NLM ID: | 101475730 |
| CIT File ID: | 14516 |
| CIT Live ID: | 6224 |
| Permanent link: | http://videocast.nih.gov/launch.asp?14516 |
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Enhanced Audio Podcast | 1:08:55 |
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Enhanced Video Podcast | 1:08:55 | |