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A20 acts as a regulator of the ectodysplasin-A1 (show EDA Proteins) pathway to NF-kappaB (show NFKB1 Proteins) activation in primary Sjogren's syndrome salivary glands epithelial cells
knockdown of A20 in tumor site inhibited tumor growth at least through inducing the apoptosis of MDSCs. A20 might be a potential target in anticancer therapy.
A20 targets caspase-8 and FADD to protect HTLV-I-infected cells.
Recruitment of A20 to the C-terminal domain of NEMO (show IKBKG Proteins) represents a novel mechanism limiting NF-kappaB (show NFKB1 Proteins) activation by NEMO (show IKBKG Proteins), and its absence results in autoinflammatory disease.
Our findings indicate that a genetic variant of TNFAIP3 is strongly associated with the silica-induced profibrotic response of fibroblasts.
There was no significant difference in PFS and OS in patients with or without A20 mutations.
Increased A20 expression is associated with cholangiocarcinoma.
FOXP1 (show FOXP1 Proteins), TP53INP1, TNFAIP3, and TUSC2 (show TUSC2 Proteins) were identified as miR (show MLXIP Proteins)-19a targets.
Loss-of-function mutations in TNFAIP3 leading to A20 haploinsufficiency cause an early-onset autoinflammatory disease.
Hepatitis C virus antigen stimulation up-regulates A20/A20-binding inhibitor of NF-kappaB (show NFKB1 Proteins) binding protein expression, which consequently contributes to inefficient M1 macrophage polarization.
MiR (show MLXIP Proteins)-221 directly targets A20, a master regulator of NF-kappaB (show NFKB1 Proteins) and MAPK (show MAPK1 Proteins) signaling, and thus represses inflammatory signaling. Restoration of A20 in macrophages abolished the stimulatory effect of miR (show MLXIP Proteins)-221 on production of proinflammatory cytokines.
Our results show that miR (show MLXIP Proteins)-873 elevates A20 levels and inhibits morphine-induced macrophage apoptosis.
a significant influence of Tnfaip3 depletion on the expression of Tsc22d3 (show TSC22D3 Proteins), Pex7 (show PEX7 Proteins), Rap2a (show RAP2A Proteins), Slc2a3 (show SLC2A3 Proteins), and Gap43 (show GAP43 Proteins) in stress response
we propose a mechanism of action by which A20 expression in club cells controls inflammation and antiviral cytotoxic T cell responses in response to influenza virus infection.
TNFAIP3 restricts MTOR (show FRAP1 Proteins) signaling and promotes autophagy, providing new insight into the manner in which MTOR (show FRAP1 Proteins) and autophagy regulate survival in CD4 (show CD4 Proteins) T cells.
autophagy downregulates A20 in F4/80hi macrophages through p62-associated autophagic sequestration and that the resulting NFkappaB activation induces expression of chemokines at an early stage of Candida infection
Up-regulated A20 promotes proliferation, regulates cell cycle progression and induces chemotherapy resistance of acute lymphoblastic leukemia cells.
A20 knockout mice develop spontaneous intestinal defects.
Data show the characterization and deduced amino acid sequence analysis for A20 gene which expression increases in MDBK cells infected by BVDV-1. Also, regulatory regions for NF-kappaB (show NFKB1 Proteins) and Sp-1 (show SP1 Proteins) additionally to an ARE element for mRNA stability were detected
This gene was identified as a gene whose expression is rapidly induced by the tumor necrosis factor (TNF). The protein encoded by this gene is a zinc finger protein and ubiqitin-editing enzyme, and has been shown to inhibit NF-kappa B activation as well as TNF-mediated apoptosis. The encoded protein, which has both ubiquitin ligase and deubiquitinase activities, is involved in the cytokine-mediated immune and inflammatory responses. Several transcript variants encoding the same protein have been found for this gene.
tumor necrosis factor, alpha-induced protein 3
, OTU domain-containing protein 7C
, TNF alpha-induced protein 3
, putative DNA-binding protein A20
, tumor necrosis factor alpha-induced protein 3
, tumor necrosis factor inducible protein A20
, zinc finger protein A20
, tumor necrosis factor induced protein 3