IndraLab

Statements



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"CARD11, CD79A/B, TNFAIP3, and MYD88 are BCR signaling components, mutation of any of them would drive alternative signaling pathway activation."

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"The up-regulation of Tnfaip3 in this paper may contribute to restoring the balance of the NF-κB signaling pathway and preventing excessive signal transduction caused by activation of the NF-κB pathway."

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"The downstream negative feedback regulators TNFAIP3 and NFKB1A were also upregulated, which may further inhibit the activation of NF-κB signaling pathway."

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"In addition, the downstream negative feedback regulator TNFAIP3 was upregulated, which may further inhibit the activation of the NF-κB signaling pathway."

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"As downstream genes of TNF, TNFAIP3 and TNFAIP6 may be overexpressed to activate the TNF-α signalling pathway."

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"In primary colorectal cancers, cancer cells reportedly activated resident fibroblasts in distal organs by releasing integrin-like 1 (ITGBL1)-rich sEV into circulation through the TNFAIP3-mediated NF-κ[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"However, the down-regulation of miR-128-2-5p expression significantly suppressed the activation of T cells and the NF-κB signaling pathway, which was mediated by TNFAIP3, further alleviating the RA symptom."

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"Ji et al. (2020) indicated that, in a CRC model, CRC extracellular vehicles (EVs) rich in integrin β-like 1 activated tumor necrosis factor α-induced protein 3 (TNFAIP3) mediated the NF-κB signaling pathway to activate CAFs, and then the CAFs released pro-inflammatory cytokines such as interleukin-6 (IL-6) and interleukin-8 (IL-8) to promote CRC metastasis."

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"Besides cytokines, Ji et al. discovered that primary colorectal tumors release integrin beta-like 1 (ITGBL1)-enriched EVs, which stimulate the TNFAIP3-mediated NF-κB signaling pathway to activate remote fibroblasts and transform them into CAFs."

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"Moreover, TNFAIP3 has been reported to control NF-kappa B activity and promote liver regeneration by activating the inflammatory IL-6/STAT3 signaling pathway."

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"The previous view suggested that ITGBL1-enriched EVs stimulate the activation of the TNFAIP3-mediated NF-κB signaling pathway in fibroblasts to prepare a favorable microenvironment for colorectal cancer metastasis or metastatic growth (Ji et al., 2020)."