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1 HCV RNA could not be restored by isoprenoid intermediate metabolites.
2 ic balances or inferred from the labeling of intermediate metabolites.
3 t stable fluxes, hence avoiding depletion of intermediate metabolites.
4 al inner mitochondrial wall transporters for intermediate metabolites.
5 eled carbon fractional enrichment values for intermediate metabolites.
6 ealed the accumulation of medicarpin and its intermediate metabolites.
7 ne followed by electron rearrangement giving intermediate metabolite 2,7-DAM, and then trapping this
8 e activation (IMA) architecture, in which an intermediate metabolite activates transcription of pathw
9 lar, we find that pathways controlled by the intermediate metabolite activation (IMA) architecture, i
11 aintaining a sufficiently large inventory of intermediate metabolites and processing units required f
13 uppresses CYP7A1, leading to accumulation of intermediate metabolites at the branch point of the meva
14 agate elsewhere into metabolic networks, and intermediate metabolites can be freely shared by differe
15 ophan metabolism in liver and brain returned intermediate metabolite concentrations in the physiologi
16 cating intracellular dThd to be an essential intermediate metabolite for the synthesis of thymine-der
17 sterol biosynthesis and the formation of the intermediate metabolites geranylgeranylpyrophosphate (GG
19 concerning fluctuations in the abundance of intermediate metabolites in various common motifs of the
20 vary in their ability to detoxify the active intermediate metabolite of AFB(1), AFB(1)-exo-8,9-epoxid
21 asma membrane are determined by an important intermediate metabolite of dietary fat and an enzyme sys
23 llular Ca2+ stores and leading to release of intermediate metabolites of arachidonic acid metabolism.
24 ause inhibiting FAS leads to accumulation of intermediate metabolites of fatty acid biosynthesis, we
25 the SLC22A1 locus for serum acylcarnitines, intermediate metabolites of mitochondrial oxidation whos
27 in hepatocytes, raising the possibility that intermediate metabolites of very long-chain fatty acids
30 that can overburden the cell and accumulate intermediate metabolites, resulting in reduced product t
31 lation of acetyl-CoA to form malonyl-CoA, an intermediate metabolite that plays a pivotal role in the
32 aldehydes and acids (FTUALs and FTUCAs) are intermediate metabolites that form from the biotransform
33 he biotransformation of FTOHs and PAPs yield intermediate metabolites that have been observed to cova
34 s controlled by a feedback mechanism between intermediate metabolites, the redox state of the plastid
35 CYP1A1 can also produce highly carcinogenic intermediate metabolites through oxidation of polycyclic
37 ery-duplicating constraint, namely, that all intermediate metabolites used in active reactions must b
38 However, an accumulation in R2 of undegraded intermediate metabolites (volatile fatty acids, ketones,
39 midazo[4,5,1-ij]quinolin-2(1H) -one [(R)-6], intermediate metabolites, where N-demethylation to the i
40 a able to degrade such a wide variability of intermediate metabolites while limiting other strains.
41 study was to assess the reactivity of these intermediate metabolites with a series of nucleophilic a
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