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The pathogenic mechanisms of SLE, which encourage Th1 cell differentiation and excessive production of IFN- and result in treatment resistance, are likewise associated with the enhancement of FAS (231)

RGFP966 increases the acetylation level of NF-B p65 at Lys122 by inhibiting HDAC3 activity to reduce collagen deposition in a UUO/IRI-induced renal fibrosis mouse model

doi: 10.3988/jcn.2016.12.1.21

Tania Dempsey: Sensitivity to Salicylates in Mast Cell Activation Disease
