IndraLab
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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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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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"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."