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1 hrough activation of Nrf2 by stabilizing the Nrf2 protein.
2 f oxidants induce de novo translation of the NRF2 protein.
3 in failed to inhibit H(2)O(2) from elevating Nrf2 protein.
4 d that H(2)O(2) increased the translation of Nrf2 protein.
5 ed in the leucine zipper (ZIP) domain of the Nrf2 protein.
6 nd hKeap1 is reduced by competition with the Nrf2 protein.
7 lls resulted in the enhanced accumulation of Nrf2 protein.
8 p1 also controls the total cellular level of Nrf2 protein.
9 r of antioxidant defences is provided by the Nrf2 protein.
10 ing binding sites on Kelch for mVP24 and the Nrf2 proteins.
11         DI-1859 induces a robust increase of NRF2 protein, a CRL3 substrate, in mouse liver and effec
12 or CUL3 by short interfering RNA resulted in NRF2 protein accumulation in vivo.
13 ed TGF-beta1-induced apoptosis and decreased NRF2 protein along with expression of its target genes.
14 PKB)/Akt pathway markedly reduced endogenous Nrf2 protein and decreased to 10-50% of normal the level
15                                 Increases in Nrf2 protein and mRNA are blocked by inhibitors of CYP2E
16 pressing HepG2 cells (E47 cells), increasing Nrf2 protein and mRNA levels, Nrf2 nuclear translocation
17                                 Increases in Nrf2 protein and mRNA were observed in livers or hepatoc
18 oxygenation-specific nuclear accumulation of Nrf2 protein and subsequent activation of a NQO1 promote
19 120 abolishes the capacity of E2 to increase NRF2 protein and transcriptional activity.
20                                        INrf2-Nrf2 proteins are sensors of chemical/radiation stress.
21 kinase were able to abolish the induction of Nrf2 protein by H(2)O(2).
22 repression of Bach1 and up-regulation of the Nrf2 protein by post-transcriptional site(s) of action.
23  formation were directly proportional to the Nrf2 protein concentration.
24        Consequently, there is an increase in Nrf2 protein degradation and a reduction in Nrf2 target
25                    Ablation of PPIA promotes NRF2 protein degradation and blocks NRF2-driven growth i
26 itination and subsequent proteasome-mediated NRF2 protein degradation.
27 tes MuSC quiescence maintenance by promoting Nrf2 protein degradation.
28                                          The NRF2 protein exhibited increased levels and more nuclear
29 T allele was associated with a low extent of NRF2 protein expression (P = 0.0003; OR, 2.420; CI, 1.49
30 on of other NOX isoforms was not altered but NRF2 protein expression was reduced under both basal and
31                           Arsenic stabilized Nrf2 protein, extending the t(1/2) of Nrf2 from 21 to 20
32 thermore, KPNA6 accelerates the clearance of Nrf2 protein from the nucleus during the postinduction p
33 th 50 microm CdCl(2) increased the amount of Nrf2 protein in a time-dependent manner; induction was o
34 sults showed that RAC3 bound directly to the Nrf2 protein in the nucleus.
35  levels: in Keap1-null MuSCs from male mice, Nrf2 protein is at an intermediate level due to the acti
36 w that an E-box-mediated circadian rhythm of NRF2 protein is essential in regulating the rhythmic exp
37       Consistent with inactivation of Keap1, Nrf2 protein is stabilized and present in the nucleus wi
38                         Without intact DJ-1, Nrf2 protein is unstable, and transcriptional responses
39                                     Cellular Nrf2 protein level and mRNA level increased in all treat
40 (+/+) mice, manifesting as increased nuclear Nrf2 protein level and Nrf2 target gene expression.
41 atment caused a rapid increase in endogenous Nrf2 protein level in rat cardiomyocytes.
42 loheximide prevented H(2)O(2) from elevating Nrf2 protein level, RNA synthesis inhibition with actino
43                             Furthermore, the Nrf2 protein levels and antiapoptotic and antioxidant en
44 NF-kappaB-deficient cells demonstrated lower NRF2 protein levels and basally impaired NRF2 signature
45 e PI3K inhibitor, NVP-BKM120, both decreased NRF2 protein levels and sensitized NFE2L2 or KEAP1-mutan
46 ell lines and show that KSHV latency induces Nrf2 protein levels and transcriptional activity through
47                    LPS stimulation increased Nrf2 protein levels in a Myd88-dependent manner.
48           Previously, it has been shown that NRF2 protein levels increase after oxidative stress beca
49       Multifaceted regulatory mechanisms for Nrf2 protein levels or activity have been mapped to its
50                                              Nrf2 protein levels, nuclear localization, and transcrip
51  Overexpression of DJ-1 results in increased Nrf2 protein levels, promotes its translocation into the
52 nt in a sex-specific manner via differential Nrf2 protein levels: in Keap1-null MuSCs from male mice,
53                      Non-electrophilic Keap1-Nrf2 protein-protein interaction (PPI) inhibitors may ha
54 ation through direct modulation of the KEAP1-NRF2 protein-protein interaction is being increasingly e
55 uncharged macrocyclic inhibitor of the Keap1-Nrf2 protein-protein interaction, a particularly challen
56  suppression is a consequence of direct ATF3-Nrf2 protein-protein interactions that result in displac
57 iferase reporter, while expression of mutant Nrf2 protein repressed activity.
58 y in FECD CECs compared with normal, whereas Nrf2 protein repressor, Keap1, was unchanged at baseline
59                           Putative conserved NRF2/protein skinhead-1 binding sites were found in AMPK
60                              Measurements of Nrf2 protein stability excluded the possibility of Nrf2
61        Our study demonstrates that targeting NRF2 protein stability is an actionable therapeutic appr
62 on the acetylation sites, with no effects on Nrf2 protein stability, compromised the DNA-binding acti
63 ofactor, is also able to negatively regulate NRF2 protein stability.
64 dylprolyl isomerase A (PPIA) is required for NRF2 protein stability.
65 rotein stability excluded the possibility of Nrf2 protein stabilization.
66                                              Nrf2 protein stabilizer, DJ-1, decreased significantly i
67 te level of Nrf2 mRNA or the initial rate of Nrf2 protein synthesis but increased the half-life of Nr
68  increased Nrf2 by decreasing degradation of Nrf2 protein (t(1/2) from 2.5 h to 9 h).
69                ZMYND8 increased stability of NRF2 protein through KEAP1 silencing.
70 hase, therefore promoting restoration of the Nrf2 protein to basal levels.
71 induces the nuclear translocation of phospho-Nrf2 protein to regulate the expression of antioxidative
72 H treatment caused a significant increase in Nrf2 protein, transcript expression, Nrf2-DNA binding ac
73 hanism of cellular defense involving de novo NRF2 protein translation governed by the EF1a interactio
74 erent 14-mer long phospho-peptides mimicking NRF2 protein using computer-based, biophysical, and bioc
75  determined the interaction between RAC3 and Nrf2 proteins using a co-immunoprecipitation assay and f
76                          Diquat induction of Nrf2 protein was higher in dwarf mice than in controls.