Fig. 5: UGT2B28 KO display lower inflammation mediators in circulation.
From: Extensive metabolic consequences of human glycosyltransferase gene knockouts in prostate cancer
a LOX and CYP/sEH-derived oxylipins are lower in UGT2B28 KO than gene-proficient controls. COX-derived oxylipins are not changed relative to control cases blue squares: lower oxylipin; full name and quantitative metabolomics data are provided in Supplementary Table S4B. b The pro-inflammatory peptides HWESASLLR and the bradykinin, derived from the kallikrein–kinin system, are lower in UGT2B28 KO; Levels of c lysophosphatidylethanolamine and d lysophosphatidylcholine in control and UGT2B28 KO cases. The median (line) and mean (+) values are indicated in boxplots. *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001. ns not significant, LOX lipoxygenase, COX cyclooxygenase, CYP cytochrome P450, sEH soluble epoxyhydrogenase, AA arachidonic acid, ALA α-linolenic acid, DGLA dihomo-γ-linolic acid, DHA docosahexanoic acid, DPA doocosapentanoic acid, EPA eicosapentanoic acid, LA linoleic acid, LPC lysophosphatidylcholine, LPE lysophosphatidylethanolamine. Quantitative metabolomics data for B, C and D are provided in Supplementary Table S3A.
