IndraLab

Statements



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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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"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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"Similarly , deficiency in CYLD or A20 , a master regulator of NFkappaB , lead to overt pathway activation and inflammation ( 132 ) ."

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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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"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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"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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"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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"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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"Collectively, we infer that TNFAIP3 relieves neuronal injury in epilepsy by suppressing inflammation."

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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 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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"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 inhibited inflammatory response and enhanced autophagy, thereby alleviating PD in mice."

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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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"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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"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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"A previous study suggested that TNFAIP3 could prevent ICH caused damaging inflammation of the brain."

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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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"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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"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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"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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"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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"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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"TNFAIP3 Reduction-of-Function Drives Female Infertility and CNS Inflammation."

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"Thus , BRO might prevent excessive inflammation also by upregulation of TNFAIP3 ."

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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 inhibited inflammatory response and enhanced autophagy , thereby alleviating PD in mice ."

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"TNFAIP3 inhibits inflammatory response and promotes extracellular matrix expression in human NPCs."

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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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"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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"In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS induced human NPCs."

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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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"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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"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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"TNFAIP3 has been found to limit inflammation and perform as an apoptosis mediator."