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Hepatitis C virus core protein ligates gC1qR (show C1QBP Proteins) to induce A20 expression in macrophages via P38 (show CRK Proteins), JNK (show MAPK8 Proteins) and NF-kappaB (show NFKB1 Proteins) signaling pathways, which leads to a low-grade chronic inflammation during HCV infection.
Results show that TNFAIP3 expression is regulated by miR (show MLXIP Proteins)-19b through targeting its 3'-UTR which contributes to the radioresistance of nasopharyngeal carcinoma and consequently activating the NF-kappaB (show NFKB1 Proteins) pathway.
demonstrates that TNFAIP3 gene polymorphisms (rs2230926 and rs5029937) are associated with the increased risk of rheumatoid arthritis. [META-ANALYSIS]
CHN1 and TNFAIP3 are candidate biomarkers for esophageal squamous cell carcinomas
These results identify the ubiquitin-editing enzyme A20 as a novel endogenous mechanism for negative regulation of fibrotic response intensity
Our data propose an additional novel mechanism to explain the known NF-kappaB inhibitory effects of A20: by affecting p105 ubiquitination and subsequently its degradation and limited processing.
A20 promotes metastasis of aggressive basal-like breast cancers through multi-monoubiquitylation of Snail1 (show SNAI1 Proteins).
Low TNFAIP3 expression is associated with colitis-associated colorectal cancer.
The miR-17-92 is a critical contributor to CML (show BCR Proteins) leukemogenesis via targeting A20 and activation of NF-kappaB (show NFKB1 Proteins) signaling.
IM could upregulate A20 protein to inhibit the activation of NF-kappaB (show NFKB1 Proteins) pathway in Jurkat T cells, which was independent of the ABIN1 (show TNIP1 Proteins) protein.
These results suggest that Leishmania exploits A20 and UCP2 (show UCP2 Proteins) to impair inflammasome activation for disease propagation
holding thymic production of natural Treg cells in check, A20 integrates Treg cell activity and increased effector T cell survival into an efficient CD4 (show CD4 Proteins)(+) T cell response
these studies establish A20 as a crucial hepatoprotective factor.
These results suggested that A20 is involved in regulating intracerebral hemorrhage-induced inflammatory injury in both the central and peripheral system
the ubiquitin-modifying enzyme TNFAIP3/A20, an upstream regulator of T cell receptor (TCR) signaling in T cells, is an essential cell-intrinsic regulator of Natural killer T differentiation.
these data reveal a crucial role of A20 in regulating the immunomodulatory activities of mesenchymal stem cells.
Therefore, A20 acts as a novel endogenous regulator of STAT1 (show STAT1 Proteins) that prevents onset of enthesitis.
This study demonstrated that miR (show MLXIP Proteins)-136-5p affected the expression of A20 in IL-17 (show IL17A Proteins)-stimulated astrocytes.
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