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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Abstract 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.
AbstractList 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.
Audience Academic
Author Sun, Shao-Cong
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  orcidid: 0000-0001-7353-9400
  surname: Sun
  fullname: Sun, Shao-Cong
  email: ssun@mdanderson.org
  organization: Department of Immunology, The University of Texas MD Anderson Cancer Center, MD Anderson UT Health Graduate School
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32205879$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1084/jem.20111703
10.1101/cshperspect.a036418
10.1038/s41556-019-0324-3
10.1016/j.celrep.2015.11.009
10.1038/s41590-020-0621-9
10.1016/j.immuni.2013.03.008
10.1038/s41590-020-0634-4
10.15252/embr.201338305
10.1126/science.289.5488.2350
10.1111/j.1600-065X.2012.01100.x
10.1016/j.molcel.2011.09.015
10.1111/imr.12308
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SubjectTerms 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
Title A20 restricts inflammation via ubiquitin binding
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