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Functional assays revealed that overexpression of MLL1 activated the TRIF/NF-κB signaling pathway, resulting in accelerated migration and invasion, and inflammation of RA-FLSs in vitro. TLR4 knockdown could compromise the effects of MLL1 overexpression. The in vivo assays in a collagen-induced arthritis rat model validated the in vitro findings. Taken together, histone methyltransferase MLL1 induces TLR4 expression by mediating H3K4me3 in the TLR4 promoter, thus activating the TRIF/NF-κB signaling pathway, which thereby promotes the mig