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Prior-Knowledge Description Expectation Prediction Conclusion Leaf Statistics
UCR01978 (S)-3-hydroxy-3-methylglutaryl-CoA + CoA = H(2)O + acetoacetyl-CoA + acetyl-CoA None - {{∅}} None - {{∅}} Unexplained
UCR02082 (R)-mevalonate + CoA + 2 NADP(+) = (S)-3-hydroxy-3-methylglutaryl-CoA + 2 H(+) + 2 NADPH None - {{∅}} None - {{∅}} Unexplained
UER00101 (R)-mevalonate from acetyl-CoA: step 1/3~2 acetyl-CoA => 1 CoA + 1 acetoacetyl-CoA. True - {{t}} True - {{t}} Confirmed presence
UCR00238 2 acetyl-CoA = CoA + acetoacetyl-CoA True - {{t}} True - {{t}} Confirmed presence
UER00102 (R)-mevalonate from acetyl-CoA: step 2/3~1 H(2)O + 1 acetoacetyl-CoA + 1 acetyl-CoA => 1 (S)-3-hydroxy-3-methylglutaryl-CoA + 1 CoA. None - {{∅}} None - {{∅}} Unexplained
UPA00058 (R)-mevalonate biosynthesis~Biosynthesis of mevalonic acid, a six-carbon metabolic intermediate. In eukaryotes, it arises from linkage of two acetyl-CoAs in the mitochondrion to form acetaoacetyl-CoA (4 carbons), followed by addition of another acetyl group from a third acetyl-CoA to give 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA). This latter compound is reduced by HMG-CoA reductase in the endoplasmic reticulum, using two NADPHs, with coincident loss of CoASH. HMG-CoA reductase is the most important regulatory enzyme for the cholesterol biosynthetic pathway and other isoprenoids/terpenoids. HMG-CoA reductase is a target for drugs that attempt to lower cholesterol levels in the body. One such drug is lovastatin, which inhibits the enzyme and stops endogenous synthesis of cholesterol. None - {{∅}} None - {{∅},{t}} Unexplained
UER00103 (R)-mevalonate from acetyl-CoA: step 3/3~1 (S)-3-hydroxy-3-methylglutaryl-CoA + 2 H(+) + 2 NADPH => 1 (R)-mevalonate + 1 CoA + 2 NADP(+). None - {{∅}} None - {{∅}} Unexplained
ULS00039 (R)-mevalonate from acetyl-CoA None - {{∅}} None - {{∅},{t}} Unexplained