A20 restricts inflammation via ubiquitin binding

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.

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Bibliographic Details
Published inNature immunology Vol. 21; no. 4; pp. 362 - 364
Main Author Sun, Shao-Cong
Format Journal Article
LanguageEnglish
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
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Summary: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.
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ISSN:1529-2908
1529-2916
1529-2916
DOI:10.1038/s41590-020-0632-6