
IndraLab
Statements
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"Administration of TPT or SN-38, a biological active metabolite of irinotecan [ xref , xref ], strongly interfered with the TNFα-induced expression of IL8 , NFKBIA (NF-κB inhibitor α), TNFAIP3 (TNFα Induced Protein 3) and ICAM1 (intercellular adhesion molecule 1), while inhibition of CXCL2 and CXCL10 expression was less pronounced ( xref C)."
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"Strikingly, Gerber’s lab has recently shown that the transcriptional cooperation between GR and NF-κB constitutes the main mechanism explaining the augmentation of TNF-induced A20 expression by dexamethasone (i.e., TNFAIP3, TNF alpha induced protein 3) in airway epithelial and smooth muscle cells ( xref ; xref )."
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"Together, these data suggest that TNFα signaling via TNFR2 promotes the expression of the anti-inflammatory mediator TNFAIP3/A20, which seems to prevent IL-17A expression in regulatory T cells, as ablation of TNFα signaling suppresses TNFAIP3/A20 and results in increased IL-17A expression in human Treg."
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"However, mutating the O-GlcNAcylation site of c-Rel or treating cells with PUGNAc has no effect on TCR or TNF-α induced expression of TNFAIP3 (encodes TNF-α induced protein 3) and NFKBIA (encodes NF-κB inhibitor α), genes that are considered to contain c-Rel binding sites in their promoters ( xref )."
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"The acod1 gene was involved in the inhibition of the inflammatory response and acted as a negative regulator of the Toll-like receptors (TLRs)-mediated inflammatory innate response by stimulating the tumor necrosis factor alpha-induced protein TNFAIP3 expression via reactive oxygen species in lipopolysaccharide-tolerized macrophages [48,49]."
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"Thirty‐eight genes involved in the defense response to virus, including bone marrow stromal antigen (BST2)/tetherin and MX Dynamin Like GTPase 2/myxovirus resistance protein 2 (MX2) and tumor necrosis factor‐alpha‐induced protein 3 (TNFAIP3) were overexpressed in VKC (Table 1 and Figure 1)."
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"The most significant increase in gene expression was of ACOD1; ACOD1 is also called IRG1 and the long non-coding RNA of ACOD1 is involved in the inhibition of the inflammatory response (Luan and Medzhitov, 2016), and also serves as a negative regulator of the TLR-mediated inflammatory innate response by stimulating the tumor necrosis factor alpha-induced protein TNFAIP3 expression via reactive oxygen species in LPS-tolerized macrophages (Li et al., 2013)."