IndraLab
Statements
TNFAIP3 inhibits inflammatory response. 35 / 38
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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 ."
eidos
"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 ."
reach
"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."
eidos
"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 ."
reach
"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]."