Tumor Necrosis Factor alpha-Induced Protein 3
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Subject Areas on Research
- A20 in Myeloid Cells Protects Against Hypertension by Inhibiting Dendritic Cell-Mediated T-Cell Activation.
- A20 modulates lipid metabolism and energy production to promote liver regeneration.
- A20 protects endothelial cells from TNF-, Fas-, and NK-mediated cell death by inhibiting caspase 8 activation.
- A20 protects from CD40-CD40 ligand-mediated endothelial cell activation and apoptosis.
- A20 protects mice from D-galactosamine/lipopolysaccharide acute toxic lethal hepatitis.
- A20 protects mice from lethal liver ischemia/reperfusion injury by increasing peroxisome proliferator-activated receptor-alpha expression.
- A20 protects mice from lethal radical hepatectomy by promoting hepatocyte proliferation via a p21waf1-dependent mechanism.
- A20, a modulator of smooth muscle cell proliferation and apoptosis, prevents and induces regression of neointimal hyperplasia.
- African-derived genetic polymorphisms in TNFAIP3 mediate risk for autoimmunity.
- Autophagy enhances NFκB activity in specific tissue macrophages by sequestering A20 to boost antifungal immunity.
- Combined expression of A1 and A20 achieves optimal protection of renal proximal tubular epithelial cells.
- Dimerization and ubiquitin mediated recruitment of A20, a complex deubiquitinating enzyme.
- Expression of A20 by dendritic cells preserves immune homeostasis and prevents colitis and spondyloarthritis.
- Genetic engineering of a suboptimal islet graft with A20 preserves beta cell mass and function.
- Genomic correlates of variability in immune response to an oral cholera vaccine.
- HIF-1α inducing exosomal microRNA-23a expression mediates the cross-talk between tubular epithelial cells and macrophages in tubulointerstitial inflammation.
- Targeting A20 decreases glioma stem cell survival and tumor growth.
- The Ubiquitin-Modifying Enzyme A20 Terminates C-Type Lectin Receptor Signals and Is a Suppressor of Host Defense against Systemic Fungal Infection.