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1 tracking is integral to the structure at the substrate level.
2 ense oligonucleotides in the presence of low substrate level.
3 reased enzyme activity and not to changes in substrate level.
4 ells were correlated with >50% reductions in substrate levels.
5 nd contribution to the control of conjugated-substrate levels.
6 ovide a complete model for the enzyme at all substrate levels.
8 doxin, which increases the efficiency of the substrate level and electron transport phosphorylations.
9 reference, adapting to the prevailing plasma substrate levels and hormonal milieu, but in type 1 diab
10 rs to run with a constant speed at different substrate levels and, therefore, is a substantial criter
11 A (alpha-GalA) activities, glycosphingolipid substrate levels, and in vitro mutation expression were
12 tate production and a significant portion of substrate-level ATP produced anaerobically, were tested
15 t mammalian antioxidant, is regulated at the substrate level by cysteine, which is synthesized from h
17 unded plants, but that the AOS hydroperoxide substrate levels, controlled by upstream enzymes (lipoxy
18 rometry-based enzyme functional analysis and substrate level-controlled enzyme kinetics consistently
19 tegy that allows acetic acid removal without substrate-level (de)phosphorylation may instead be emplo
20 the effects of metabolite concentrations and substrate-level enzyme regulation while identifying meta
21 rial oxidative phosphorylation, increases in substrate level generation of ATP and reducing equivalen
23 relates with lowered pERK but unchanged pPKA substrate levels in D1 medium spiny neurons as well as i
25 associated negative PE occurred even at low substrate levels in this study could be attributed to li
27 tive interventions aiming at alleviating the substrate-level inhibition of key enzymes in order to en
28 idic operations, instrument portability, and substrate-level integration with other pre- and post-PCR
29 proteasome inhibition, and this increase in substrate level is consistent with the observed loss of
30 zation of genome-annotated, respiratory, and substrate-level lactate dehydrogenases (LDHs) from the o
31 erability of DA neurons and that enhancing G-substrate levels may be a neuroprotective strategy for t
32 e the complete inhibition of MOC, indicating substrate level phosphorylation and explicit anaerobic s
33 ondrial enzyme capable of ATP production via substrate level phosphorylation in the absence of oxygen
36 robically generate ATP by intramitochondrial substrate-level phosphorylation and maintain DeltaPsi(m)
38 ctions and is not fermentative, we find that substrate-level phosphorylation is its primary anaerobic
40 ed cells with Embden-Meyerhof glycolysis and substrate-level phosphorylation that lack the alpha-prot
42 tron acceptors, generates ATP primarily from substrate-level phosphorylation under anaerobic conditio
44 ive phosphorylation via the pmf, but also by substrate-level phosphorylation via the enzyme AckA.
45 te as the electron acceptor, consistent with substrate-level phosphorylation yielding a significant a
46 asses (e.g., fermentation pathways bypassing substrate-level phosphorylation), substrate channeling (
47 ding carbon fixation, the shikimate pathway, substrate-level phosphorylation, gluconeogenesis and gly
54 is significantly higher than of disulfides, substrate level regulation favors the synthesis of H2S o
56 ranscriptional and translational regulation, substrate-level regulation of enzyme activity, post-tran
58 conditions of reduced mitogen or nutritional substrate levels, the serine/threonine kinase target of
60 suggest that the early kinetic events at the substrate level ultimately govern successful chaperonin-
61 ne was adaptively regulated by extracellular substrate level via transcriptionally mediated mechanism
63 enzyme); conversely, when the intracellular substrate level was reduced by methionine deprivation, t
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