Figure S3 Replicate quality analysis plot for the amino acid profiling by UPLC-LC-MS/MS in the mutant stock SALK_021108 (AT1G52670). Instructions in how to interpret this plot can be found in the consortium web portal (Figure taken from www.PlantMetabolomics.com). The numbers in the upper right corner correspond to the correlation coefficients between replicates (ith row, jth column). The x (ith replicate) and y (jth
replicate) coordinates of the scatterplots are the logarithms (base 2) of the ratio of the mean relative abundances (μ) of each amino acid in the wild-type (wt) versus mutant (mt) plant (i.e., log2 (μmt/uwt)). Conflict of Interest Conflict of Interest The Inhibitors,research,lifescience,medical authors declare no conflict of interest.
Arachidonic acid is metabolized to an array of oxidized bioactive lipids by a series of different oxygenases
that can introduce molecular oxygen with extraordinary regioselectivity and stereospecificity (Figure 1). Free arachidonic acid serves as the substrate for cyclooxygenases Inhibitors,research,lifescience,medical (COXs), lipoxygenases (LOXs), and cytochromes P-450 (CYPs); whereas esterified arachidonic acid is primarily metabolized by 15-LOX-1. The ability of COXs to convert arachidonic acid to prostaglandins Inhibitors,research,lifescience,medical (PGs) and thromboxane A2 was recognized over 50 years ago [1,2,3]. Two COX isoforms have been identified, the first of which, COX-1, is Luminespib chemical structure constitutively active [4]. The presence of a second inducible form of COX was first suggested by experiments, which showed a transient increase in the formation of PGE2 from arachidonic acid by canine kidney cells upon stimulation Inhibitors,research,lifescience,medical with tumor promoters and carcinogens [5,6]. The increased PGE2 production was eliminated by inhibition of transcription or translation, Inhibitors,research,lifescience,medical indicating that it was dependent upon de novo COX synthesis. This new isoform (COX-2)
was subsequently cloned, sequenced, and its expression was found to be inducible in human cells [7]. COX-2 and COX-1 share 60% sequence homology [8] and they are both responsible for the metabolism of free arachidonic acid to the bioactive only PGs and TXA2 (Figure 1). Figure 1 Pathways of arachidonic acid metabolism. Abbreviations: COX, cyclooxygenase; CYP, cytochrome P540; EET, epoxyeicosatrienoic acid; EH, epoxide hydrolase; FLAP, 5-lipoxygenase activating protein; GGT, γ-glutamyltranspeptidase; GSH, glutathione; … Arachidonic acid is converted initially to the hydroperoxy-endoperoxide PGG2, which subsequently converts to the hydroxy-endoperoxide PGH2 through the enzyme’s peroxidase (POX) activity (Figure 1) [9]. A variety of bioactive arachidonic acid metabolites are produced from PGH2, varying in function from regulating inflammation, blood clotting, ovulation, initiation of labor, bone metabolism, nerve growth and development, kidney function, and blood vessel tone.