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A20 may be a potential therapeutic target for DLBCL.
There is a significantly higher occurrence of the A20 rs143002189 polymorphism in diffuse large B cell lymphoma (DLBCL) compared to non-neoplastic controls and other types of B cell malignancies.
HMBA was able to increase prostratin-induced phosphorylation and degradation of NF-kappaB (show NFKB1 ELISA Kits) inhibitor IkappaBalpha (show NFKBIA ELISA Kits), thereby enhancing and prolonging prostratin-induced nuclear translocation of NF-kappaB (show NFKB1 ELISA Kits), a prerequisite for stimulation of transcription initiation
A Japanese family case with juvenile onset Behcet's disease caused by TNFAIP3 mutation.
TNFAIP3 gene polymorphisms (rs9494885 and rs7753873) are associated with the susceptibility to allergic rhinitis in the Chinese Han population.
A20 significantly inhibited poly(I:C)-induced cytokine production, and this effect was related to the inhibition of NF-kappaB (show NFKB1 ELISA Kits) signaling. These results suggest that the downregulation of A20 increased the susceptibility of keratinocytes to external stimuli, thus contributing to the development of psoriasis.
we indentified 13 susceptibility SNPs and a long risk haplotype for SLE at TNFAIP3 gene locus. Our results suggest that TNFAIP3 is a susceptible gene for SLE in Han Chinese population.
By using bioinformatics analysis tool (Targetscan), the 3' untranslated region (3'UTR (show UTS2R ELISA Kits)) of A20 gene was found to be a target of miR (show MLXIP ELISA Kits)-125a. The expression level of miR (show MLXIP ELISA Kits)-125a in pancreatic cancer tissues from chemo-sensitive patients was significantly lower than that from chemo-resistant patients, and was inversely correlated with the A20 mRNA.
Data suggest an association of TNFAIP3 SNPs with susceptibility to chronic ITP (show ITPA ELISA Kits). Together with previous reports, finding provides further evidence for TNFAIP3 being a general autoimmunity gene.
we identify the single nucleotide polymorphism rs2327832 of TNFAIP3 as a possible prognostic marker for diabetes outcome in children with T1D.
Forced expression of A20 resulted in decreased expression of key markers of lipogenesis and adipogenesis, such as sterol regulatory element binding protein (show CNBP ELISA Kits) 1c (SREBP-1c (show SREBF1 ELISA Kits)) and adipogenesis (aP2 (show TFAP2A ELISA Kits)), leading to less lipids accumulation in differentiated 3T3-L1 cells
these results suggest that Mycobacterium fortuitum-induced activation of host proinflammatory responses is negatively regulated through TLR2 (show TLR2 ELISA Kits)-dependent A20 expression.
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.
MiR (show MLXIP ELISA Kits)-221 directly targets A20, a master regulator of NF-kappaB (show NFKB1 ELISA Kits) and MAPK (show MAPK1 ELISA Kits) signaling, and thus represses inflammatory signaling. Restoration of A20 in macrophages abolished the stimulatory effect of miR (show MLXIP ELISA Kits)-221 on production of proinflammatory cytokines.
A20 targets caspase-8 and FADD to protect HTLV-I-infected cells.
Our results show that miR (show MLXIP ELISA Kits)-873 elevates A20 levels and inhibits morphine-induced macrophage apoptosis.
a significant influence of Tnfaip3 depletion on the expression of Tsc22d3 (show TSC22D3 ELISA Kits), Pex7 (show PEX7 ELISA Kits), Rap2a (show RAP2A ELISA Kits), Slc2a3 (show SLC2A3 ELISA Kits), and Gap43 (show GAP43 ELISA Kits) 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 ELISA Kits) signaling and promotes autophagy, providing new insight into the manner in which MTOR (show FRAP1 ELISA Kits) and autophagy regulate survival in CD4 (show CD4 ELISA Kits) 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
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 ELISA Kits) and Sp-1 (show SP1 ELISA Kits) 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