Abstract
Although known for many years as a nuclear factor (NF)-κB inhibitory and antiapoptotic signaling protein, A20 has recently attracted much attention because of its ubiquitin-regulatory activities and qualification by genome-wide association studies (GWASs) as a susceptibility gene for inflammatory disease. Here, we review new findings that have shed light on the molecular and biochemical mechanisms by which A20 regulates inflammatory signaling cascades, and discuss recent experimental evidence characterizing A20 as a crucial gatekeeper preserving tissue homeostasis.
Keywords:
A20; apoptosis; inflammation; nuclear factor-κB; tumor necrosis factor α-induced protein 3; ubiquitination.
Copyright © 2013 Elsevier Ltd. All rights reserved.
Publication types
-
Research Support, Non-U.S. Gov't
-
Review
MeSH terms
-
Animals
-
Autoimmunity*
-
B-Lymphocytes / immunology
-
B-Lymphocytes / metabolism
-
Cell Death
-
DNA-Binding Proteins / deficiency
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / metabolism*
-
Disease Models, Animal
-
Enzyme Activation
-
Gene Targeting
-
Genetic Predisposition to Disease
-
Host-Pathogen Interactions / immunology
-
Humans
-
Immunity, Innate
-
Inflammation / etiology
-
Inflammation / immunology*
-
Inflammation / metabolism*
-
Intestinal Mucosa / immunology
-
Intestinal Mucosa / metabolism
-
Intracellular Signaling Peptides and Proteins / deficiency
-
Intracellular Signaling Peptides and Proteins / genetics
-
Intracellular Signaling Peptides and Proteins / metabolism*
-
Mice
-
Myeloid Cells / immunology
-
Myeloid Cells / metabolism
-
NF-kappa B / metabolism
-
Nuclear Proteins / deficiency
-
Nuclear Proteins / genetics
-
Nuclear Proteins / metabolism*
-
Skin / immunology
-
Skin / metabolism
-
Tumor Necrosis Factor alpha-Induced Protein 3
Substances
-
DNA-Binding Proteins
-
Intracellular Signaling Peptides and Proteins
-
NF-kappa B
-
Nuclear Proteins
-
TNFAIP3 protein, human
-
Tumor Necrosis Factor alpha-Induced Protein 3