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this study shows that functional variants of TNFAIP3 are associated with systemic lupus erythematosus in a cohort of Chinese Han population
Staphylococcus epidermidis-induced interleukin-1 beta and beta-defensin-2 expression in keratinocytes is regulated by the host molecule A20 (TNFAIP3) and may help S. epidermidis to persist on human skin.
results implicate TNFAIP3 as a functionally important endogenous suppressor of ASK1 hyperactivation in the pathogenesis of nonalcoholic steatohepatitis (NASH) and identify it as a potential new molecular target for NASH therapy
Activation of ligand-inducible chimeric FGFR1 (iFGFR1) upregulated TNFAIP3 in an ERK2-dependent manner and TNFAIP3 is required for iFGFR1 activation-promoted ductal carcinoma in situ (DCIS) cell proliferation, tumor growth and progression. Knockout of TNFAIP3 blocks FGFR1 signaling-promoted DCIS cell proliferation suggesting that TNFAIP3 is required for FGFR1 signaling-promoted DCIS growth and progression.
TNFalpha contributes to the aggressive properties of triple negative breast cancer cell lines via upregulation of A20. A20 mediates pleiotropic effects of TNFalpha playing role in aggressive behaviors of TNBC subtype while its deficiency results in TNFalpha-induced apoptotic cell death in luminal breast cancer subtype.
these results suggest that MYD88L265P signaling can be enhanced by a second genetic alteration in TNFAIP3 and highlights a potential opportunity for therapeutic targeting.
The expression of MiR-128-3p was significantly increased, while TNFAIP3 was decreased, the levels of IL-6 and IL-17 were also increased in the T cells of rheumatoid arthritis patients.
this study postulate that deregulation of the NF-kappaB pathway as a result of the TNFAIP3 rs2230926 aberration increases Sjogren's syndrome susceptibility
This study showed that the expression of A20 was decreased in Behcet's disease (BD) patients with active uveitis but not in Vogt-Koyanagi-Harada (VKH) disease. Decreased expression of A20 may lead to an enhanced activation of proinflammatory Th17 cells, causing a reactivation of BD.
expression loss of A20 protein and gene detection of TNFalpha inducing protein 3 are found in both EBV negative and positive patients with Hodgkin's lymphoma
Our data suggest that ABIN1 protects human leukaemia T-cells by allowing them to resist the apoptosis induced by T. gondii ME-49 and that the T. gondii ME-49 strain induces the apoptosis of human leukaemia T-cells via A20-mediated downregulation of ABIN1 expression.
Our findings suggest that a disruption of the normal function of the TNFAIP3 gene might serve as a therapeutic target for the treatment of brucellosis.
Findings suggest that A20 is critical for proper functioning of the DDR in cancer cells and it establishes a new link between this NFkappaB-regulated ubiquitin-editing enzyme and the DDR pathway.
The miR-29a-3p may act as a tumor promotive miRNA by regulating cells migration through directly targeting of A20 gene in human gastric epithelial cells infected with H.pylori.
A significant association was found between anxiety and TNFAIP3 mRNA levels in patients with major depressive disorder.
Single nucleotide polymorphisms in ITGAM, TNFSF4, TNFAIP3 and STAT4 genes are associated with susceptibility to systemic lupus erythematosus in a North Indian population.
Expressed and isolated a recombinant fusion cell penetrating TAT-A20 protein, and observed its inhibitory effect on TNFalpha-induced NF-kappaB activation in cultured cells.
Analysis of postmortem brain tissue and CSF of multiple sclerosis (MS) patients revealed that expression of A20/TNFAIP3, as well as the expression levels of IL-1beta and NLRP3 were significantly increased in MS plaques.
LIFR-AS1 serves as a competitive endogenous RNA for miR-29a to inhibit its expression and up-regulate downstream target TNFAIP3 expression, finally modulating the resistance of colorectal cancer to pohotodynamic therapy.
Study demonstrates evidence of the constitutive expression of A20 in macrophages, its role in supporting the differentiation program, and the functional consequences of the zinc finger domains thereof.
These data show that the disease susceptibility proteins A20 and ABIN-1 synergistically prevent intestinal inflammation by restricting IEC death and preserving tissue integrity.
Several inflammatory proteins were found up-regulated in the absence of A20, even without an inflammatory stimulus, but, depending on the treatment, more proteins were found regulated. Together these protein changes may affect normal signaling events, which may disturb tissue homeostasis and induce (autoimmune) inflammation, in agreement with A20s proposed identity as a susceptibility gene for inflammatory disease.
Study data show that the anti-inflammatory protein A20 and the critical autophagic mediator Atg16l1 physically interact and synergize to regulate the stability of the intestinal epithelial barrier. Collectively data show that A20 and Atg16l1 cooperatively control intestinal homeostasis by acting at the intersection of inflammatory, autophagy and cell death pathways.
Overexpression of tumor necrosis factor alpha-induced protein 3 (A20) in mice reduces the colitis activity index score and the histological score of the intestine. A20 decreases inflammatory cytokine levels in the intestine and increases colon length. A20 overexpression downregulates the activation of NF-kB and STAT3. A20 improves colitis through suppression of Th17 cells differentiation.
It has been proposed that ABIN-1 provides a critical link between methionine1 ubiquitylation mediated by the LUBAC complex and lysine63 deubiquitylation by phospho-A20 to modulate the activation of RIPK1.
M protein of Group A streptococcus was responsible for inducing A20 expression in murine macrophages.
In mice, deletion of A20 in microglia increases microglial cell number and affects microglial regulation of neuronal synaptic function. Microglia A20 deficiency also exacerbates multiple sclerosis-like disease, due to hyperactivation of the Nlrp3 inflammasome leading to enhanced interleukin-1beta secretion and CNS inflammation.
A20 dimers bind linear ubiquitin to stabilize the Ripoptosome and potentiate its apoptosis-inducing activity.
At least in the subcutaneous fat of humans and mice, the levels of PGC-1a decrease during obesity, while its physical association with A20 increases.
T cell-specific A20 limited the expansion but reduced apoptosis and necroptosis of Listeria-specific CD8(+) T cells, resulting in an impaired pathogen control in primary but improved clearance in secondary infection.
study reveals a critical role of IL-17RC in maintaining baseline A20 production and a novel role of the IL-17RC-A20 axis in controlling JNK isoform-dependent tumor-specific homeostatic proliferation.
Deletion of TT>A enhancer results in inflammatory arthritis.
The data demonstrate that miR-125b regulates nasopharyngeal carcinoma cell proliferation and apoptosis by targeting A20/NF-kappaB signaling pathway, and miR-125b acts as oncogene, whereas A20 functions as tumor suppressor.
Mice with A20 deficient B cells are prone to food allergy.
Tnfaip3, an anti-inflammatory gene, is located precisely underneath the linkage peak and contains two non-synonymous SNPs leading to conservative amino acid substitutions.
Hepatitis C virus core protein ligates gC1qR to induce A20 expression in macrophages via P38, JNK and NF-kappaB signaling pathways, which leads to a low-grade chronic inflammation during HCV infection.
These results suggest that Leishmania exploits A20 and UCP2 to impair inflammasome activation for disease propagation
A20 promotes metastasis of aggressive basal-like breast cancers through multi-monoubiquitylation of Snail1.
holding thymic production of natural Treg cells in check, A20 integrates Treg cell activity and increased effector T cell survival into an efficient CD4(+) T cell response
these studies establish A20 as a crucial hepatoprotective factor.
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 and Sp-1 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