https://www.selleckchem.com/products/r16.html
O3-induced pro-inflammatory gene expression for CXCL2 and CXCL8/IL8 was further enhanced in NLRP2 knockout cells, suggesting a negative regulatory role. Reconstitution of NLRP2 KO cells with K1019R mutant NLRP2 partially blocked SecoA adduction and enhanced O3-induced IL-8 release as compared to wild type NLRP2. Together, our findings uncover NLRP2 as a highly abundant, key component of pro-inflammatory signaling pathways in airway epithelial cells and as a novel mediator of O3-induced inflammation. Rapid advances in cochlear implantation h
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