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USP3 inhibits NFASC. 6 / 6
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"To identify the molecular target of USP3, we co‐transfected USP3 with different signaling proteins in the NF‐κB pathway and found that USP3 mainly inhibited MyD88‐induced NF‐κB activation and slightly but significantly inhibited TRAF6‐induced NF‐κB activity only at a high USP3 concentration (Fig 3A)."
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"Using the USP3 and USP3 cells, we found that USP3 deficiency enhanced the NF‐κB activation induced by MyD88 and TRAF6, but not by IKKα or IKKβ (Fig 3C)."
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"Ectopic expression of USP3 inhibited the NF‐κB activation induced by MyD88 in USP3 cells (Fig 3D)."
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"LPS priming resulted in the cytoplasmic retention of USP3, which enabled it to remove the K63‐linked polyubiquitin chains more efficiently on MyD88 and attenuate subsequent NF‐κB signaling upon a second LPS challenge."
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"Using USP3‐transfected cells treated with IL‐1β (a ligand for IL‐1R), TNFα (a ligand for TNFR), or 293T‐TLR4 cells treated with LPS (a ligand for TLR4), we showed that USP3 potently inhibited the NF‐κB activation induced by LPS and IL‐1β (Fig 1B)."
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"To determine whether USP3 could inhibit different types of TLRs‐mediated NF‐κB activation, we tested the secretion of NF‐κB‐responsive cytokines after stimulation with different TLR ligands: Pam CSK (a ligand for TLR1/2), LPS, and CL‐097 (a ligand for TLR7/8)."
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