A20 restricts inflammation via ubiquitin binding

• Published in: Nature immunology Vol. 21; no. 4; pp. 362 - 364
• Main Author: Sun, Shao-Cong
• Format: Journal Article
• Language: English
• Published: New York Nature Publishing Group US 01.04.2020; Nature Publishing Group
• Subjects: 631/250/249/2510/2511; 631/250/256/2515; 631/250/262; Arthritis; Arthritis, Psoriatic; Biomedical and Life Sciences; Biomedicine; Cellular signal transduction; Chronic illnesses; Cytokines; Enzymes; Genetic aspects; Genotype & phenotype; Health aspects; Humans; Immunology; Infections; Infectious Diseases; Inflammation; Inflammatory diseases; Lymphatic system; Lymphocytes; Mutation; News & Views; news-and-views; Physiology; Protein Binding; Senescence; Tumor Necrosis Factor alpha-Induced Protein 3; Tumor necrosis factor-TNF; Ubiquitin; Ubiquitin-proteasome system; Ubiquitins; Viruses; United States

The ubiquitin-editing enzyme A20 has a pivotal role in restricting autoimmune and inflammatory responses. New studies suggest that A20 prevents inflammatory diseases using a non-catalytic mechanism involving ubiquitin binding.