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TNFAIP3 inhibits inflammatory response. 59 / 62
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"A variant of TNFAIP 3, which encodes an ubiquitin editing enzyme inhibiting NF-kappaB-dependent signaling and prevents inflammation, and polymorphic haplotypes of the human T-lymphotropic virus-1-related endogenous sequence (HRES) 1 long terminal repeat (LTR) have been associated with SLE [XREF_BIBR, XREF_BIBR]."
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"Tnfaip3 deficiency causes spontaneous CNS inflammation characterised by microglial activation and induction of inflammatory mRNAs in the brain (54)."
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"TNFAIP3 is particularly important to maintain homeostatic NFkappaB activation and suppress inflammation in the intestinal milieu where mucosal surfaces are constantly exposed to luminal bacteria."
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"Tnfaip3 expression is necessary for prevention of chronic inflammation and autoimmune pathology according to studies on mice with full or conditional gene deletion [XREF_BIBR]."
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"55 , 56 In oral cavity, partial TNFAIP3 loss or impaired expression leads to increased gingival inflammation in oral mucosa."
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"TNFAIP3 inhibited inflammatory response and enhanced autophagy, thereby alleviating PD in mice."
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"Additionally, the same group has reported that TNFAIP3 can endogenously suppress ASK1 and reduce apoptosis, lipid accumulation, and inflammation [XREF_BIBR]."
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"A20 Restricts Inflammatory Response and Desensitizes Gingival Keratinocytes to Apoptosis The pathophysiology of periodontal disease involves a perturbed immune system to a dysbiotic microflora leading to unrestrained inflammation , collateral tissue damage , and various systemic complications ."
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"Deletion of tnfaip3 gene in mice lead to die prematurely due to severe inflammation and cachexia and are more responsive to LPS and TNF [ 79 ]."
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"The use of TNFAIP3 siRNA further increased inflammatory mediators and reduced permeability proteins, suggesting that increasing TNFAIP3 levels may reduce retinal inflammation."
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"Lee EG et al. described that TNFAIP3-deficient mice could trigger a spontaneous inflammation, cachexia, and embryonic death [ 39 ]."
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"TNFAIP3 is involved in the cellular response to H O and negatively regulates B cell activation, the CD40 signaling pathway, inflammatory response, and the death domain receptor exogenous apoptosis signaling pathway [41,42,43,44]."
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"Using acute and chronic HDMs-driven asthma models, Vroman et al. recently found that conditional deletion of Tnfaip3 gene in mouse myeloid cells promotes the secretion of Th17-inducing cytokines IL-1β, IL-6, and IL-23, thereby increasing Th17 cell numbers and exacerbating neutrophilic inflammation (18)."
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"Given the greater repression of inflammation by A20 compared to ABIN1 , we sought to understand whether keratinocytes in psoriasis and other rashes display upregulation of the A20 repressed gene sets discovered in our NHEK experiments ."
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"TNFAIP3 is an inhibitor of TNF-alpha inflammatory response via NF-kappaB and protects cells from TNF induced apoptosis, through inhibition of the caspase cascade and by prevents endothelial cell activation XREF_BIBR."
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"TNFAIP3 reduces inflammation, glucose metabolism disorders and lipid accumulation by inhibiting the activation of apoptotic signal-regulated kinase 1 ( ASK1 ) in liver cells ( Liu et al., 2020 )."
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"Numerous researchers have identified that A20 is a susceptibility gene for inflammatory diseases , and that A20 inhibits inflammation by regulating the NF-kappaB pathway.17-21 Interestingly , when NF-kappaB translocates into the nucleus and binds to the kappaB binding site in the A20 gene promoter structure , it can promote the expression of the A20 gene , and A20 acts as an ubiquitinating enzyme to modify the upstream molecules of the NF-kappaB pathway , leading to a negative feedback loop between A20 and the NF-kappaB ."
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"In mice, the overexpression of TNFAIP3 inhibits NLRP3 inflammasome complex, preventing lupus inflammation and renal injury ( 53 )."
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"A panel of 10 inflammatory cytokines and expression of TNFAIP3 (A20; inhibits NF-kappabeta-induced inflammation) were analyzed in duodenal and ileal biopsies."
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"TNFAIP3 is known to reduce the inflammatory response by strongly inhibiting TNF-a/NF-kB signaling [29] ."
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"Collectively, we infer that TNFAIP3 relieves neuronal injury in epilepsy by suppressing inflammation."
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"Reduced TNFAIP3 expression leads to prolonged activation of NF-κB, resulting in increased inflammation and autoimmunity [60,61]."
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"Furthermore, TNFAIP3 is activated by NF-kappaB in response to pro inflammatory signals such as TNF-alpha and can inhibit inflammation and programmed cell death."
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"We have previously shown that deficiency of Tnfaip3 in macrophages renders these cells hypersensitive to IL-33 stimulation (Holgado et al., 2023) and now report that basophil deficiency of this asthma susceptibility gene increases basophil activation, numbers, and subsequent eosinophilic airway inflammation."
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"Likewise, a correlation between increased H3 acetylation and transcript expression levels was observed among upregulated genes, for example, for the NF-κB negative regulator TNFAIP3, which plays a piv[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"A20 has been implicated in negatively regulating NF-κB signalling, cell death and inflammasome activation; however, the mechanisms by which A20 inhibits inflammation in vivo remain poorly understood."
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"TNFAIP3 has been found to limit inflammation and perform as an apoptosis mediator."
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"These results supported that A20 could inhibit the inflammatory response via regulating NF-κB activation in hepatic injury models in vitro ."
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"In vivo and in vitro experiments indicated that inflammation , a key characteristic of epilepsy , was inhibited by TNFAIP3 upregulation , as evidenced by the downregulated expression of pro-inflammatory cytokine interleukin ( IL ) -1 beta and inducible NO synthase ( iNOS ) , along with the decreased levels of NLRP3 inflammasome , which could activate inflammation ."
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"Altogether, A20 inhibited NF-κB-mediated inflammatory response without influencing or even could be taken as the mediator of its hepatoprotective function xref , xref , xref , xref ."
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"TNFAIP3 is primarily responsible for attenuation of NFkappaB signaling and thereby inhibits inflammation and tumorigenesis and TNF mediated mediated apoptosis [XREF_BIBR]."
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"Results demonstrated that TNFAIP3 knockdown contributed to the proliferation ( Fig. 5b ) , migration ( Fig. 5d ) , invasion ( Fig. 5e ) , and inflammation ( Fig. 5f ) and suppressed the apoptosis ( Fig. 5c ) in HAND2-AS1-overexpressed MH7A cells ."
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"Furthermore, miR-218-5p in CMs-EVs from DCM patients can activate the TGF-β signaling and increase fibrosis-related gene expression by inhibiting the master inflammation inhibitor TNFAIP3 in CFs, which results in expanded fibrosis and impaired cardiac function when these EVs are injected into mice hearts (Fu et al. 2023)."
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"Given the fact that A20 can inhibit inflammation, and as TNF-α-associated intestinal inflammation is a pivotal factor in IBD pathogenesis, we explored the correlation between TNF-α production, A20 expression, and disease status."
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"Taken together, A20 inhibited FFAs-induced inflammatory response via attenuating NF-κB activation in four cell lines we generated."
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"axis likely plays a role in SARS-CoV-2 infection as well, with TNFAIP3 inhibiting NF-κB-mediated antiviral responses at the site of local infection yet promoting a systemic inflammatory response in the periphery."
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"On one hand, TNFAIP3 can reduce the progression of inflammation‐related tumors."
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"Cell type specific roles for TNFAIP3 in intestinal inflammation have been demonstrated by lineage specific deletions showing that TNFAIP3 mainly suppresses inflammation in myeloid cells , while it mainly suppresses cell death in intestinal epithelial cells ( IEC ) 11 ."
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"This indicates that melatonin treatment can increase the expression of TNFAIP3, thereby suppressing the inflammation (Fig. 6A)."
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"Melatonin treatment can increase the expression of TNFAIP3, thereby suppressing inflammation."
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"In conclusion, the experimental results indicate that melatonin treatment can increase the expression of TNFAIP3, thereby suppressing inflammation."
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"TNFAIP3 inhibited inflammatory response and enhanced autophagy , thereby alleviating PD in mice ."
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"In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS induced human NPCs."
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"TNFAIP3 Reduction-of-Function Drives Female Infertility and CNS Inflammation."
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"However, in samples with high promoter methylation, TNFAIP3 expression was downregulated, which may weaken the inhibition of NF-κB and TNF-α pathways, leading to enhanced inflammation (Yang et al., 2011)."
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"One mechanism by which A20 inhibits inflammation is through negative regulation of NLRP3 and caspase-1 activation , suppressing interleukin production and pyroptosis ( 167 , 168 ) ."
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"The repression of TNFAIP3 enhanced inflammation that would further magnify fibrogenic effects in CFs.Taken together, the results of this study explored a new mechanism of Exos-mediated profibrotic effect in familial DCM."
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"Similarly , deficiency in CYLD or A20 , a master regulator of NFkappaB , lead to overt pathway activation and inflammation ( 132 ) ."
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"Elevated expression of Tnfaip3 can inhibit the progression of inflammation during an inflammatory attack.In this study, we analyzed the changes in immune cells in ALI and their interrelationships."
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"In COPD airway epithelium , influenza virus infection increased microRNA-125a / b , which directly inhibits A20 and mitochondrial antiviral-signaling protein ( MAVS ) to promote inflammation and impair antiviral responses in COPD ( 84 ) ."
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"Although TNFAIP3 functions to limit inflammation, our finding of chlamydial plasmid-encoded Pgp3 protein augmented TNFAIP3 agrees with a previous report which infected HeLa cells using plasmid-bearing C. trachomatis [21]."
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"As a stress response gene in endothelial cells (ECs), TNFAIP3/A20 has a protective effect against tumor necrosis factor (TNF)-mediated apoptosis, and inhibits inflammation."
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"Indeed, Tnfaip3 critically restricts CNS microglia activation and microglia-dependent inflammation (54, 55)."
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"In vivo and in vitro experiments indicated that inflammation, a key characteristic of epilepsy, was inhibited by TNFAIP3 upregulation, as evidenced by the downregulated expression of pro-inflammatory cytokine interleukin (IL)-1β and inducible NO synthase (iNOS), along with the decreased levels of NLRP3 inflammasome, which could activate inflammation."
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"Thus , BRO might prevent excessive inflammation also by upregulation of TNFAIP3 ."
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"TNFAIP3 inhibits inflammatory response and promotes extracellular matrix expression in human NPCs."
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"Additionally, SOCS1, a critical suppressor of Th1 cytokine production ( Palmer and Restifo, 2009 ) and TNFAIP3 which limits inflammation via NFkB inhibition ( Li, 2011 ), were over-expressed."
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"A previous study suggested that TNFAIP3 could prevent ICH caused damaging inflammation of the brain."
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"The results of this study showed that TNFAIP3 significantly reduces inflammatory response and ameliorates the degradation of the extracellular matrix by promoting autophagy in LPS-induced-inflammatory human NPCs that mimics IVDD."
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