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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.
this meta-analysis confirms that TNFAIP3 gene polymorphisms may play important roles in the pathogenesis of Rheumatoid arthritis
Report a significant association between the biased usage of IGHV4-34 (binds to the carbohydrate I/i antigens) and inactivating mutation of TNFAIP3 [encoding a global negative regulator of the canonical nuclear factor-kappaB (NF-kappaB (show NFKB1 Proteins)) pathway] in ocular adnexal MALT lymphomas.
TNFAIP3 rs10499194 T allele and CT genotype were associated with an increased risk for AIH-1 (show AMELX Proteins)
Haploinsufficiency of TNFAIP3 (A20) by a germline heterozygous mutation leads to the autoimmune lymphoproliferative syndrome (ALPS) phenotype.
These results suggested that A20 is involved in regulating intracerebral hemorrhage-induced inflammatory injury in both the central and peripheral system
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.
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.
Our data suggest that NAOs have a beneficial preventive effect in septic shock correlated with the enhancement of IL-10 (show IL10 Proteins) via the induction of A20 and COX-2.
Forced expression of A20 resulted in decreased expression of key markers of lipogenesis and adipogenesis, such as sterol regulatory element binding protein (show CNBP Proteins) 1c (SREBP-1c (show SREBF1 Proteins)) and adipogenesis (aP2 (show TFAP2A Proteins)), leading to less lipids accumulation in differentiated 3T3-L1 cells
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