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"Furthermore, recently evidence showed different types of PCD existed extensive crosstalk and could even switch to each other under specific conditions.31, 32, 33 A20 (the tumor necrosis factor alpha-induced protein 3, TNFAIP3) has been shown to enhance autophagy and reduce pyroptosis in PDLCs."
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"Another study by Ji et al. found that CRC-derived integrin beta-like 1 (ITGBL1)-rich sEVs stimulate the tumor necrosis factor alpha-induced protein 3 (TNFAIP3)-mediated NF-κB signaling pathway to activate fibroblasts, which in turn induce PMN formation and promote metastasis by secreting pro-inflammatory cytokines (e.g."
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"Tumor Necrosis Factor Alpha-Induced Protein 3 (TNFAIP3), a zinc finger protein and ubiquitin editing enzyme, inhibits NF-κB activation and apoptosis induced by cytokines such as TNF-α and IL-1β or via Toll-like receptors (TLRs) and is involved in immune and inflammatory responses."
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"LMP1 activates mitogenic NF-κB signaling pathways to increase metastasis through activation of matrix metalloproteinases (MMP9) [66], promote cell proliferation through epidermal growth factor receptor (EGFR) [67] induction, stimulate the anti-apoptotic gene tumor necrosis factor alpha-induced protein 3, TNFAIP3 [68], and modulate the expression of chemokines and chemokine receptors (CXCL9, CXCL10, CX3CL1, and CCL20) [69]."
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"The RA susceptibility gene A20, also called tumor necrosis factor alpha-induced protein 3 gene (TNFAIP3), is a cytokine-inducible protein that inhibits apoptosis and activates NF-κB. A20-deficient mice were prone to spontaneous erosive arthritis, which was found to be related to elevated NLRP3 expression and IL-1β secretion (87)."
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"XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR Tumor necrosis factor alpha induced protein 3 (TNFAIP3, also known as A20), functioning as an ubiquitin editing enzyme, 15 negatively regulates NF-kappaB signaling through dual mechanisms, that is, deconjugation of K63 linked polyubiquitin chains from RIP-1 and subsequent conjugation of RIP-1 with K48 linked polyubiquitin chains for proteasomal degradation."
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"Transcriptome analysis and further experimental confirmation in MDA-MD-231 cells revealed that forced overexpression of CTCF might attenuate the DNA binding ability of nuclear factor-kappaB (NF-kappaB) p65 subunit and inhibit activation of NF-kappaB and its target pro oncogenes (tumor necrosis factor alpha induced protein 3 [TNFAIP3]) and genes for growth related proteins (early growth response protein 1 [EGR1] and growth arrest and DNA-damage-inducible alpha [GADD45a])."
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"Focusing on the link between the inflammatory response and the activation of HSCs will help us further explore the mechanisms by which liver fibrosis occurs.A20, also known as tumor necrosis factor alpha-induced protein 3 (TNFAIP3), is a cytoplasmic zinc finger protein that encodes an ubiquitin-editing enzyme."
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"In addition, increased expression of IFN inducible transcription factors STAT1 and STAT2, TNF-alpha induced protein TNFAIP3, apoptosis related proteins caspase3 and caspase4, suppressors of cytokine signaling Socs1 and Socs3, pro inflammatory cytokines IL-1 and IL-6, TLR7, as well as IFN response antiviral genes of OAS family were also observed in microarray analysis."
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"This study investigated the potential combined influence of PPARalpha, tumor necrosis factor alpha induced protein 3 (TNFAIP3 and A20), and tumor necrosis factor receptor associated factor 6 (TRAF6) on interleukin (IL)-12p40 production by macrophages exposed to DEHP and stimulated with lipopolysaccharide (LPS)."
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"The hypoxia-inducible factor 1α (HIF-1α; obtained from Wuhan Fine Biotech Co., Ltd. Wuhan, China), NFκB p65 Total/Phospho (NFκB p65 Total/Phospho; obtained from Thermo Fisher Scientific, CA, USA), and A20 (Rat Tumor Necrosis Factor Alpha Induced Protein 3(TNFaIP3) or A20 obtained from Wuhan Xinqidi Biological Technology, China) were assessed in the cell lysates isolated from OHCs."
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"TNF-alpha induces TNFAIP3, tumor necrosis factor-alpha-induced-protein 3 which is also known as A20, TNFAIP3 interacts with TNIP1 gene encoded TNFAIP3 interacting protein 1 (TNIP1 protein), TNFAIP3 and TNIP1 then in conjunction regulate NF-kappaB dependent gene expression negatively."
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"Thus, we distinguish the pathologies mediated by IL-1 family cytokines (e.g., the case of FMF or mevalonate-kinase deficiency), the diseases of interferon production and signaling called interferonopathies [e.g., Aicardi-Goutières syndrome and STING-associated vasculitis with onset in infancy (SAVI)], and the diseases of NFkB activation [e.g., Blau syndrome and haploinsufficiency of A20/tumor necrosis factor alpha-induced protein 3 (TNFAIP3)]."
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"NF-kappaB signaling is controlled by negative feedback via IkappaBalpha and A20 and TNIP2 (tumor necrosis factor alpha induced protein 3 [TNFAIP3] in chicken) transcriptional induction [XREF_BIBR] and we found TNFAIP3 mRNA and protein unchanged but IkappaBalpha mRNA decreased, suggesting that this negative feedback mechanism is suppressed."
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"A multi-progenitor meta-analysis identified 34 novel loci (P < 5e-8) and newly discovered candidate genes, including tumor necrosis factor alpha-induced protein 3 (TNFAIP3) interacting protein 2 (TNIP2) and TNF receptor superfamily member 11 A (TNFRSF11A), confirming the important roles of the immune system and joint tissues in the etiology of RA [13]."
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"In upregulated genes induced by IL-1β, treatment with STF (3 μg/mL) provided greater effects on downregulation of inflammatory and immune genes involved in NF-κB components (NFKB1,NFKBIA,NFKBIZ), chemokines (CCL2,CXCL1,CXCL2,IL8), transcriptional regulator (IRF1), prostaglandin E synthase (PTGES) and TNF alpha induced protein family (TNFAIP2, TNFAIP3, TNFAIP6) than indomethacin in IL-1β-treated cells."
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"In normal cells, MLL3 and MLL4 assemble complexes for establishing H3K4me1 at target enhancers or superenhancers, promoting transcription of genes related to differentiation or tumor suppression such as tumor necrosis factor alpha-induced protein 3 (TNFAIP3) and suppressor of cytokine signaling 3 (SOCS3) ."
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"The IPA analysis presented in Figure 4 demonstrates that interleukin (IL)-1α, IL32, tumor necrosis factor (TNF), TNF alpha-induced protein 3 (TNFAIP3), and toll-like receptor 2 (TLR2) are among the immune-related genes involved in this pathway and identified as targets of the generated miRNA signature."
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"We were also able to demonstrate that enteroids deficient in IL-10 show a defective activation of NFκB, with dysregulated gene expression of known downstream targets of NFκB, such as Tnf, and NFκB pathway inhibitor genes Nfkbia and Tnfaip3, encoding IκBα and A20 (tumor necrosis factor, alpha-induced protein 3, TNFAIP3), respectively [24]."
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"In a large prospective study of patients with type 1 diabetes in the USA, researchers have reported three SNPs associated with increased risk of type 1 diabetes (rs10517086_A, rs1534422_G and rs2327832_G in tumor necrosis factor, alpha induced protein 3 [TNFAIP3]) and one with decreased risk (rs1004446_A in INS) 43."
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"Tumor necrosis factor alpha-induced protein 3 (TNFAIP3) is an anti-inflammatory signaling molecule that regulates NF-κB signaling negatively and has been considered as a new druggable target that is strongly related to the fibrotic manifestations across multiple ethnic cohorts (Momtazi et al., 2019)."
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"A20, also known as the TNF-alpha-induced protein 3 (TNFAIP3), is a zinc finger protein that was first identified from a gene, TNFAIP3, that was induced by TNF-alpha in human umbilical vein endothelial cells XREF_BIBR; it is now known that A20 is widely expressed in a variety of human cells."
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"To introduce new diagnostic markers in patients with celiac disease for easy, fast, low cost, and non-invasive diagnosis, we evaluated the peripheral blood expression levels of interleukin-15 (IL-15), interleukin-17A (IL-17A), interleukin23A (IL-23A), granzyme B (GzmB), T-box transcription factor 21 (TBX21), and tumor necrosis factor alpha-induced protein 3 (TNFAIP3) of patients compared with the healthy controls, which were extracted from public databases organized in a protein-protein interaction network, in this group."
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"Trim24-repressed targets included several genes involved in inflammatory response and cell cycle regulation, including cyclooxygenase 2 (Cox2), regulator of cell cycle (Rgcc) and tumor necrosis factor alpha-induced protein 3 (TNFAIP3) (Supplementary Fig. 12f and Extended Data Fig. 2)."
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"Differential analysis was conducted on 92 significantly downregulated proteins, and it was found that these proteins contained inflammatory response-related components, such as platelet glycoprotein 4 (CD36), Interleukin-6 receptor subunit beta (IL6ST), Tumor Necrosis factor alpha-induced protein 3 (TNFAIP3), and Tumor Necrosis factor-alpha-induced protein 8-like protein 2 (TNFAIP8L2)."
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"Activating mutations that target the genes encoding the BCR subunits CD79a and CD79b, the BCR pathway adaptor caspase recruitment domain family member 11 (CARD11), and MYD88 promote NF-κB activity in ABC DLBCL, as do genetic and epigenetic events that inactivate tumor necrosis factor α–induced protein 3 (TNFAIP3, also known as A20) ."
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"Using ICRAFT, we identified numerous targets that enhance both cancer cell susceptibility to immune attack and T cell activation, including tumor necrosis factor (TNF) alpha-induced protein 3 (TNFAIP3), protein tyrosine phosphatase non-receptor type 2 (PTPN2), and suppressor of cytokine signaling 1 (SOCS1)."
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"Additionally, several deubiquitination enzymes (DUBs), including A20 (also known as tumor necrosis factor alpha induced protein 3; TNFAIP3) and the tumour suppressor, CYLD (also known as cylindromatosis), implicated in familial cylindromas, have been shown to control critical signalling steps upstream of the IKK complex [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"In addition, reduced expression was also evident for two IL17 target genes in vertebrates : tumor necrosis factor alpha induced protein 3 (tnfaip3; also known as A20), which encodes a ubiquitin editing enzyme that inhibits NF-kappaB activation, and NF-kappaB inhibitor zeta (nfkbiz), an IL17 target gene in vertebrates that also regulates NF-kappaB activity."
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"Notably, a total of seven DEGs were identified in the downregulated NF-κB signaling pathway, including chemokine C-X-C motif ligand 12 (CXCL12), CXCL2, intercellular adhesion molecule 1 (ICAM1), lymphocyte antigen 96 (LY96), nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor alpha (NFKBIA), protein inhibitor for activated stat 4 (PIAS4), and tumor necrosis factor alpha-induced protein 3 (TNFAIP3), which may play important roles in COMMD7-mediated regulation of the NF-κB signaling pathway."
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"E3 ubiquitin ligases, such as TNF-α–induced protein 3 (TNFAIP3; A20), baculoviral IAP repeat containing 2 (BIRC2; cIAP1), baculoviral IAP repeat containing 3 (BIRC3; cIAP2), tripartite motif containing 31 (TRIM31), ring finger protein 186 (RNF186), and membrane-associated ring-CH-type finger 3 (MARCH3), serve as key negative regulators in multiple signal pathways, participating in intestinal homeostasis by regulating immune response, IEC proliferation, apoptosis, or necroptosis (14–20)."
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"In patients with ACPA-negative RA, certain polymorphisms have been identified, including variants in the ankyrin repeat domain 55(ANKRD55)/interleukin 6 signal transduce (IL6ST), B lymphoid tyrosine kinase (BLK), tumor necrosis factor alpha-induced protein 3 (TNFAIP3), GIN1 protein/C5orf30 (GIN1/C5orf30), STAT4, 60S ribosomal protein pseudogene (RPL), and nuclear factor I A (NFIA)genes, suggesting that distinct genetic factors may underlie these two subsets of RA (24, 25)."
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"Prior exposure to some environmental factors and microbial contents, including farm dust, butyrate, LPS, and N-glycolylneuraminic acid, can suppress the responses of the airway epithelium to allergens because they induce the expression of TNF-α induced protein-3 (TNFAIP3, also called A20), a negative regulator of NF-κB activation (227)."
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"55 A testable hypothesis would thus be that combined innate and adaptive stimulation from certain cross-reactive commensals drive chronic autoreactivity in genetically predisposed people such as those carrying certain human leukocyte antigen (HLA) and innate immune variants (e.g. tumor necrosis factor alpha induced protein 3 or TNFAIP3)."
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"We showed that Pgp3 induced prominent expression of host inflammatory cytokine genes including interleukin-6 (IL-6), IL-8, tumor necrosis factor alpha-induced protein 3 (TNFAIP3), and chemokine C-X-C motif ligand 1 (CXCL1), implying a possible role of Pgp3 in modulating the inflammatory reaction in the host."
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"Based on the transcriptomic analysis, we identified four major categories of genes associated with the TNF signaling pathway: members of the TNF receptor superfamily (TNFRSF5, TNFRSF6B, TNFRSF16, TNFRSF18, and TNFRSF19), TNF alpha-induced proteins (TNFAIP2, TNFAIP3, and TNFAIP8), and TNF receptor-associated factors (TRAF1 and TRAF5) (Fig. 4C)."