IndraLab

Statements

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"Importantly, TNFAIP3 knockout not only inhibited the AP20187 induced proliferation and tumor growth of DCIS-iFGFR1 cells, but also further reduced baseline proliferation and tumor growth of DCIS-iFGFR1 cells without AP20187 treatment."
30111373
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"Both Emu- BCL10 and Emu- API2-MALT1 mice develop splenic marginal zone hyperplasia but not lymphoma [86,113], while TNFAIP3 (A20) deficiency in B-cells enhances B-cell proliferation with an excessive [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"In addition, the knockdown of TNFAIP3 restores the significant decrease in invasion and proliferation in miR-605-5p-inhibitor-transfected lung cancer cells."
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"However, when overexpressing TNFAIP3 and PLAU or upon activation of the NFkappaB pathway, all the inhibitory effects of SFE were reversed (XREF_FIG A-D), suggesting that SFE blocked the p65 promotion of TNFAIP3 and PLAU expression to inhibit ESCC cell proliferation and metastasis."
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"miR-29c targets TNFAIP3, inhibits cell proliferation and induces apoptosis in hepatitis B virus related hepatocellular carcinoma."
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"TNFAIP3 deficient B-cells are hyper-reactive to antigen stimulation, leading to enhanced proliferation and survival."
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"HIV-1 subsets upregulated CXCR4 and TNFAIP3, which modulate cell proliferation and initiate inflammatory immune responses, respectively."
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"Cluster 2 contained IL8, IL1A, PTGS2, DTR, TNFAIP3, and CXCL3 that were up-regulated and linked primarily to inflammatory response and cell proliferation."
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"We also demonstrate that knockout (KO) of TNFAIP3 blocks FGFR1 signaling-promoted DCIS cell proliferation and progression, suggesting that TNFAIP3 is required for FGFR1 signaling-promoted DCIS growth and progression."
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