IndraLab

Statements

TNFAIP3 inhibits IL6. 6 / 6
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"Using the MWCL-A20 and HBL-1-A20 , we were able to show that loss of TNFAIP3 enhances MYD88 -driven NF-κB and p38 signaling resulting in increased expression of NF-κB target genes IL-6 and CXCL10, known NF-κB target genes , have both been shown to be significantly upregulated in WM and DLBCL, and higher serum levels correlate with an inferior survival ."
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"However, our data indicate that this dysregulation can be further driven by TNFAIP3 loss in patients with MYD88 mutations.The importance of IL-6 and the autocrine mechanism by which IL-6 induces STAT3 activation in DLBCL has been shown in previous studies ."
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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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"This agrees with A20 inhibiting IL-6 and promoting TGFβ production by medial SMC and in SMC cultures exposed to cytokines, thereby favoring differentiation of regulatory over pathogenic T cells."
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"However, histone H3K4 methyltransferase ASH1L inhibited NF-κB signaling downstream of the TLR by promoting the expression of TNFaip3 (a negative regulator of TLR signaling pathway), thereby inhibiting macrophage production of IL-6 and TNF-α (115)."
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"Furthermore, when compared with TNFAIP3 non knockdown and UBE2L3 knockdown in human HeLa cells, TNFAIP3 knockdown and UBE2L3 non knockdown synergistically increase three cytokines, CCL2, CXCL8 (IL8), and IL6, all regulated by NF-kappaB in the human TNFR signaling pathway."
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