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1 ng protocols have consistently shown lack of enzyme induction.
2 r phosphorylation and angiotensin-converting enzyme induction.
3 anscription factor responsible for lipogenic enzyme induction.
4 fficiently high level by the slow process of enzyme induction.
5  cell extracts obtained at various stages of enzyme induction.
6 ity or evidence of hepatic biotransformation enzyme induction.
7 nflammatory activity, antiproliferation, and enzyme induction.
8  topoisomerase IIbeta, loss of antioxidative enzyme induction and attenuated protection against ODD b
9 e pools revealed a close correlation between enzyme induction and cytochrome c release, caspase activ
10 wed that a minimal model accounting only for enzyme induction and dilution captures all the substrate
11 ility to adapt to stress through antioxidant enzyme induction and translocation of these proteins to
12 ion of whether bone mass is truly related to enzyme induction, and analogously, of whether reductions
13 intain high potency and efficacy for phase 2 enzyme induction as well as the inhibitory effect on lip
14 on that agr autoactivation, unlike classical enzyme induction, can occur under suboptimal conditions
15 lation exposure, including immune responses, enzyme induction, cellular toxicity, and histopathologic
16 ha and other cytokine production, as well as enzyme induction (cyclooxygenase-2, inducible nitric oxi
17 alogue concentrations, which caused 300-fold enzyme induction in parental cells.
18 istance and activities of putative defensive enzymes, induction of defence-related genes and activati
19 ch from other laboratories on the effects of enzyme induction on chemical carcinogenesis as an approa
20 erum theophylline levels, possibly caused by enzyme induction or autoinduction.
21 which was additive to the substrate-mediated enzyme induction produced by the ingested erythrocyte he
22             Compound 4 showed a superior rat enzyme induction profile relative to compound 1, allowin
23 mechanism, whereas the Ah receptor-dependent enzyme induction reduces adducts in liver, probably due
24                                              Enzyme induction reflects increased transcription of the
25  mechanism by which TAM mediates antioxidant enzyme induction remains unclear.
26                                              Enzyme induction was found to be about 50% greater with
27 erol 7alpha-hydroxylase and initially favors enzyme induction, whereas increased bile acid pool is th
28  activation of the bkd operon by BkdR during enzyme induction which incorporates these results is pre
29     As has been observed previously, hepatic enzyme induction with PB or betaNF shifted the location