IndraLab

Statements


Lipopolysaccharide increases the amount of TNFAIP3. 14 / 14
8 | 6

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"In this study, LJF significantly inhibited the LPS stimulated downregulation of CXCL2, CXCL1, CXCL6, NFKBIA, IFNG, IL6, IL17A, IL17F, IL17C, MMP9, and TNFAIP3 mRNA expression in lung tissue homogenates according to RNA-Seq and qRT-PCR, which indicates that the IL-17 signalling pathway is critical for treatment by LJF of LPS induced ALI."
| PMC

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"The results indicate that miR-98-5p interference and 3beta-hydroxycholest-5-en-7-one treatment significantly upregulated the low TNFAIP3 expression induced by LPS stimulation, thereby inhibiting TRAF6, RIP, NF-kappaB, IL-1beta, and TNF-alpha secretion."

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"In the TREM2 + ScMglia population, expression of IL-1beta, CCL2, and TNFAIP3 were all significantly induced by LPS stimulation compared with untreated controls (XREF_FIG)."

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"LPS significantly enhanced TNFAIP3 and IRAK-M levels but reduced Sp1 levels."

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"We have proposed a working model based on these results (XREF_FIG) and suggest that Tnfaip3 might be expressed through transcriptional regulation of both p65 and the p38-downstream transcription factor C/EBPbeta in response to LPS."

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"Ex vivo farm dust or LPS stimulation restored TNFAIP3 expression to healthy levels in asthmatics and shifted NF-kappaB signaling associated gene expression towards an anti-inflammatory state (p < 0.001)."

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