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1 f oxidants induce de novo translation of the NRF2 protein.
2 lls resulted in the enhanced accumulation of Nrf2 protein.
3 hrough activation of Nrf2 by stabilizing the Nrf2 protein.
4 r of antioxidant defences is provided by the Nrf2 protein.
5 in failed to inhibit H(2)O(2) from elevating Nrf2 protein.
6 d that H(2)O(2) increased the translation of Nrf2 protein.
7 ed in the leucine zipper (ZIP) domain of the Nrf2 protein.
8 nd hKeap1 is reduced by competition with the Nrf2 protein.
9 p1 also controls the total cellular level of Nrf2 protein.
10 ing binding sites on Kelch for mVP24 and the Nrf2 proteins.
12 ed TGF-beta1-induced apoptosis and decreased NRF2 protein along with expression of its target genes.
13 PKB)/Akt pathway markedly reduced endogenous Nrf2 protein and decreased to 10-50% of normal the level
15 pressing HepG2 cells (E47 cells), increasing Nrf2 protein and mRNA levels, Nrf2 nuclear translocation
17 oxygenation-specific nuclear accumulation of Nrf2 protein and subsequent activation of a NQO1 promote
21 repression of Bach1 and up-regulation of the Nrf2 protein by post-transcriptional site(s) of action.
25 T allele was associated with a low extent of NRF2 protein expression (P = 0.0003; OR, 2.420; CI, 1.49
26 on of other NOX isoforms was not altered but NRF2 protein expression was reduced under both basal and
28 thermore, KPNA6 accelerates the clearance of Nrf2 protein from the nucleus during the postinduction p
29 th 50 microm CdCl(2) increased the amount of Nrf2 protein in a time-dependent manner; induction was o
31 w that an E-box-mediated circadian rhythm of NRF2 protein is essential in regulating the rhythmic exp
37 loheximide prevented H(2)O(2) from elevating Nrf2 protein level, RNA synthesis inhibition with actino
39 NF-kappaB-deficient cells demonstrated lower NRF2 protein levels and basally impaired NRF2 signature
40 e PI3K inhibitor, NVP-BKM120, both decreased NRF2 protein levels and sensitized NFE2L2 or KEAP1-mutan
41 ell lines and show that KSHV latency induces Nrf2 protein levels and transcriptional activity through
45 Overexpression of DJ-1 results in increased Nrf2 protein levels, promotes its translocation into the
46 suppression is a consequence of direct ATF3-Nrf2 protein-protein interactions that result in displac
48 y in FECD CECs compared with normal, whereas Nrf2 protein repressor, Keap1, was unchanged at baseline
50 on the acetylation sites, with no effects on Nrf2 protein stability, compromised the DNA-binding acti
54 te level of Nrf2 mRNA or the initial rate of Nrf2 protein synthesis but increased the half-life of Nr
57 H treatment caused a significant increase in Nrf2 protein, transcript expression, Nrf2-DNA binding ac
58 hanism of cellular defense involving de novo NRF2 protein translation governed by the EF1a interactio
59 determined the interaction between RAC3 and Nrf2 proteins using a co-immunoprecipitation assay and f
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