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by performing protein profiling on isolated astrocytes we showed that an increase in astrocytic DJ-1 expression up-regulated a large group of proteins associated with redox regulation, inflammation and mitochondrial respiration. The majority of these proteins have also been shown to be regulated by Nrf2.
Nrf2 was activated in response to the ER stress via the PERK pathway.
Knockdown of Nrf2 paralogs perturbed glutathione redox state in zebrafish embryo. Nrf2 alone is not essential for the response and recovery of glutathione to oxidative insults.
nrf2a modulates the embryonic response to perfluorooctanesulfonic acid (PFOS), and that PPAR signaling may play a role in the embryonic adaptive response to PFOS.
These results suggest that alpha,beta-unsaturated carbonyl entity and catechol moiety of 6S derivatives may react with the cysteine residues of Keap1, disrupting the Keap1-Nrf2 complex, thereby liberating and activating Nrf2. Our findings of natural product-derived Nrf2 activators lead to design options of potent Nrf2 activators for further optimization.
These data suggest that EC from the Tripterygium wilfordii stem extract could diminish tau-GFP-induced neuronal death through the activation of Nrf2.
we concluded that Nrf2 plays a fundamental and conserved role in protection against acute sodium arsenite toxicity
Coptisine exerted its antioxidant activity against AAPH-induced toxicity involving in activating Akt and JNK/Nrf2/NQO1 pathway.
Bach1 regulates the liver specificity and transience of the Nrf2a-dependent induction of hmox1a and that heme mediates this regulation through Bach1 inhibition based on its level in each tissue.
The Bach1b-MafK heterodimer represses the zymogen promoters, whereas the Nrf2a-MafK heterodimer activates them.
The expression of nrf genes varies temporally throughout development and nrf genes are induced following a pro-oxidant exposure and are potentially cross-regulated by gene family members Nrf2a and Nrf2b.
oxidative stress is an important mechanism of Cd-mediated injury in the zebrafish olfactory system; the Nrf2 pathway plays a protective role against cellular oxidative damage and is important in maintaining zebrafish olfactory function.
results revealed that nrf2 mutant zebrafish are viable and fertile but show an increased susceptibility to oxidative stress and electrophiles
compared the tissue-specific expression of several Nrf2 target genes in zebrafish larvae; Tissue-restricted induction was observed in the nose, gill, and/or liver for seven genes in response to Nrf2-activating compounds
Nrf2 is protective against PFOS-induced oxidative stress in zebrafish larvae.
mutation of either residual cysteine residue in Keap1a and Keap1b disrupted the ability of Keap1 to repress Nrf2, indicating that the presence of either Cys-273 or Cys-288 is sufficient for fish Keap1 molecules to fully function
study reports that the Keap1-Nrf2 system comprises discrete sensor sites, including the Keap1 cysteines Cys-151 and Cys-273, for a variety of Nrf2-activating compounds
findings demonstrate that antioxidant responses are a component of polycyclic aromatic hydrocarbon (PAH)synergistic developmental toxicity and that NRF2 is protective against prooxidant and PAH challenges during development
These findings suggest that bronchiolar epithelial cells and macrophages up-regulate Nrf2 expression early in the course of infection, which results in increased expression of HO-1 within these cells.
the survival and developmental competence of embryos cultured under oxidative stress are associated with activity of the NRF2-mediated oxidative stress response pathway during bovine pre-implantation embryo development.
expression of target genes in liver in transition period and stages of lactation
investigation of molecular mechanisms of microvascular complications in diabetes/hyperglycemia: Nrf2 is involved in regulation of HO-1 gene expression in aortic endothelial cells by advanced glycation end products
The results of the current study indicate that dioscin may protect against coronary heart disease by regulating oxidative stress and inflammation via Sirt1/Nrf2 and p38 MAPK pathways.
Lack of Nrf2 enhances susceptibility to mycotoxin-induced kidney disease.
The effects of ochratoxin A on the nuclear translocation and transactivation of the transcription factor Nrf2 as well as mRNA levels of Nrf2 target genes are reported.
the involvement of ATF3 and its splice variant DeltaZip2 in TGF-b1 and Nrf2-driven pancreatic tumorigenesis was investigated. As demonstrated here, PDAC cells or premalignant H6c7 pancreatic ductal epithelial cells differentially express DeltaZip2- and ATF3, relating to stronger Nrf2 activity seen in Panc1 cells and TGF-ss1 activity in T3M4 or H6c7 cells, respectively.
it was found that a potential phosphorylation of S53 affected Keap1-Nrf2 binding in the pull-down assay, and induced nuclear translocation of Nrf2 in the electrophoretic mobility shift assay.
Delivery of KEAP1 exon 2 specific Cas9:guide RNA in Jurkat T cells led to significant ( approximately 70%) editing and upregulation of NRF2-regulated antioxidant genes.
NRF1 is more stable in KEAP1(+/+) than in KEAP1(-/-) isogenic cell lines, whereas NRF2 is dramatically stabilized in KEAP1(-/-) cells.
The upstream regulators of NRF2 provide new clues on cytoplasmic irradiation-induced biological processes and prevention of radiation risks.
Review of current knowledge on Nrf2 signaling pathway, structure, and activity under both physiological state and upon oxidative stress.
Setd7 knockdown decreases Nrf2 and Nrf2-target genes expression, and phenethyl isothiocyanate and ursolic acid induce Setd7 expression, which activates the Nrf2/antioxidant response element signaling pathway and protects DNA from oxidative damage.
These results indicated that Nrf2 may have a functional in the reversal effect of curcumin and contribute, at least in part, to the outcomes of chemotherapy in patients with MDR.
Nrf2 protein expression in the esophageal squamous cell carcinoma.Aberrant signaling via the Keap1-Nrf2 pathway was common in esophageal squamous cell carcinoma and was associated with response and survival after chemoradiotherapy.
Nrf2 limits HSCs activation, through the inhibition of the TGF-beta1/Smad pathway in HSCs
NRF2 promotes syncytiotrophoblast differentiation by inducing C/EBPbeta, PPARgamma, hCYP19A1, and miR-1246, which targets WNT inhibitors and JARID2 and is dysregulated in preeclampsia.
Study found that miR1443p could regulate the cisplatin resistance of lung cancer cells via Nrf2.
Treadmill training in peripheral artery disease patients through unfolded protein response and Nrf2 up-regulation may trigger hypoxic adaptation similar to conditioning, thus modifying cell survival
Authors found that the antioxidant cinnamaldehyde activated the NRF2/HMOX1 pathway. Cinnamaldehyde also alleviated TGF-beta1- and IL-13-mediated production of reactive oxygen species and subsequent POSTN upregulation in dermal fibroblasts. NRF2 silencing abolished the cinnamaldehyde-mediated downregulation of POSTN.
While the primary tumours showed mutations in genes associated with cell adhesion and motility, brain metastases acquired mutations in adaptive, cytoprotective genes involved in response to cellular stress such as Keap-1, Nrf2 and P300, which are key players of the Keap1-Nrf2-ARE survival pathway.
The key antioxidant enzymes and transcription factor Nrf2 are up-regulated, and the NOX5 expression is reduced during development of drug resistance of tumor cells to cisplatin.
HIF1A is upregulated in breast and bladder tumors with high NRF2 activity. NRF2 targets a functional antioxidant response element at the HIF1A locus, which reveals a direct regulatory connection between two important oxygen responsive transcription factors.
A core set of 32 direct NRF2 targets that are consistently upregulated in NRF2 hyperactivated tumors.
The expression of Nrf2-ARE molecules and related antioxidases is significantly decreased in patients with OSAHS and is correlated with neurocognitive dysfunction.
These results suggest that constitutive activation of Nrf2 might be linked with tumor aerobic glycolysis and progression of UTUC, indicating that Nrf2 signaling in the tumor microenvironment promotes progression of UTUC.
A delicate and synergistical collaboration between YY1 and the master transcription factor NRF2 that functions to mobilize the cell's antioxidant machinery.
In conclusion, these results indicated that Nrf2 activation in response to hyperhomocysteinemia plays an important role in mediating homocysteine-suppressed lipolysis in adipocytes.
We have firstly evaluated in silico the genes belonging to the Nrf2/HO-1/CO pathway that are involved in the pathogenesis of autoimmune hepatitis (AIH). The data obtained from the in silico study demonstrate that a significant number of genes modulated in the liver of ConA-challenged mice belong to the Nrf2 pathway
Cold exposure induced cardiac injury by inhibiting the Nrf2-Keap1 signaling pathway.
Genetic knockout of NRF2 demonstrates its role in developmentally regulated gamma-globin gene expression and the ability to control oxidative stress and the phenotypic severity of Sickle cell disease.
Study used a gene expression biomarker that can accurately predict the activation status of the oxidant-induced transcription factor Nrf2 in a microarray database and uncovered a strong linkage between increased Nrf2 activity and feminization of the male liver mediated by suppression of STAT5b. Examination of female versus male comparisons showed that Nrf2 is subtly but reproducibly activated to higher levels in females.
SIPS reversed CTX-induced immunosuppression effectively and predominantly through Nrf2-mediated oxidative stress, which provided the useful evidence that SIPS can be served as a novel natural immunomodulator in health foods or medicine.
modulation of NF-E2-related factor 2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke
It has been shown that genetic ablation of Nrf2 abolishes an adaptive muscle NQO1 activity and catalase induction.
Study indicated that, by increasing the expression of NRF2, the mitophagy induced by melatonin provided protection against brain injury post-SAH.
Dopamine D5 receptor may play an important role in the preservation of normal heart function by inhibiting the production of reactive oxygen species, via inhibition of NADPH oxidase, Nrf2 degradation, and ERK1/2/JNK pathways.
Nrf2 signaling rescues oligodendrocytes damaged by dysfunctional mitochondria.
The Nrf2-ARE signaling pathway plays a vital role in preventing aGVHD in an HSCT mouse model by regulating the expression of the downstream antioxidant genes NQO1 and HO-1 and by inhibiting the local inflammatory reaction.
Nrf2/Keap1 system regulates VSMC apoptosis during neointimal formation, thereby inhibiting neointimal hyperplasia after a vascular injury.
H2AX has a physiologic function in mediating influences of oxidative stress on NRF2-transcriptional targets and behavior
disruption of PTEN resulted in steatohepatitis, fibrosis and caused hepatic induction of the Nrf2-dependent antioxidant system at least in part due to elevation of p62
NRF2 inhibition is effective against the progression of chemically and spontaneously induced tumors.
Ori might exhibit a protective role against H2O2-stimulated oxidative damage by the induction of HO-1 expression through the activation of the JNK- and PI3K/AKT-Nrf2 signaling pathways.
Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect.
These results indicate that loss of NRF2 activity critically worsens the inflammatory response to proteinopathy by anticipating onset and worsening progression of neuropathological cues.
This gene encodes a transcription factor which is a member of a small family of basic leucine zipper (bZIP) proteins. The encoded transcription factor regulates genes which contain antioxidant response elements (ARE) in their promoters\; many of these genes encode proteins involved in response to injury and inflammation which includes the production of free radicals. Multiple transcript variants encoding different isoforms have been found for this gene.
, nuclear factor (erythroid-derived 2)-like 2
, nuclear factor erythroid 2-related factor 2
, NF-E2-related factor 2
, NFE2-related factor 2
, nuclear factor, erythroid derived 2, like 2
, nuclear factor erythroid-derived 2-like 2
, nuclear factor erythroid 2-like 2