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"The authors further suggested that the deubiquitylation of NLRP3 was critical for the inflammasome activation based on the facts that inhibiting BRCC3 could abolish NLRP3 inflammasome activation under a diverse range of classic " activation signals, " including K + efflux, ROS overproduction, and lysosomal destabilization."
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"Our collective data supported the requirement of the VDR‐BRCC3 signaling pathway for VD3‐induced inactivation of the NLRP3 inflammasome and subsequent inhibition of hyperinflammation in HBE‐N cells.2.4
VD3 attenuated N protein-induced hyperinflammation by inactivating the NLRP3 inflammasome through the VDR-BRCC3 signaling pathway in vivo."