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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.
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.
NRF2 is a transcription factor that robustly transduces chemical signals to regulate a battery of cytoprotective genes. KEAP1 represses NRF2 activity under quiescent conditions, whereas NRF2 is liberated from KEAP1-mediated repression on exposure to stresses. [review]
the ability of porphyra-334 and shinorine to dissociate Nrf2 from Keap1 was confirmed also by measurement of increased mRNA expression of Nrf2 targeted genes encoding oxidative stress defense proteins in primary skin fibroblasts prior and post UVR exposure.
NRF2, DJ1 and SRNX1 are commonly expressed in diffusely infiltrating astrocytomas and they can be used in predicting patient prognosis.
the present findings were the first to show that pterostilbene attenuated high glucose-induced central nervous system injury in vitro through the activation of Nrf2 signaling, displaying protective effects against mitochondrial dysfunction-derived oxidative stress.
In some breast cancer cells, xCT antiporter expression is upregulated through the antioxidant transcription factor Nrf2 and contributes to their requirement for glucose as a carbon source.
study provides support for the involvement of both NFE2L2 and PPARGC1alpha in Parkinson's disease susceptibility and progression, marginally and through pathways involving maneb and paraquat exposure.
Our data suggests a novel interaction between Nrf2 and ATF4 under oxidative and endoplasmic reticulum stress, thus drives specific enzymatic and non-enzymatic reactions of antioxidant mechanisms maintaining redox homeostasis.
The senescence-associated downregulation of NRF2 decreases endothelial glycolytic activity and stress tolerance both of which are restored after reinstating NRF2.
Aberrant Nrf2/Keap1 system integrity may affect self-defence mechanisms against oxidative stress in primary biliary cholangitis.
Inflammation, oxidative stress, and higher expression levels of Nrf2 and NQO1 proteins in the airways of women chronically exposed to biomass fuel smoke.
Data suggest that NRF2/NFE2L2 promotes breast cancer progression by enhancing glycolysis through co-activation of HIF1A; NRF2 and HIF1A mRNA and protein levels are significantly up-regulated in breast cancer cells as compared to benign breast epithelial cells. (NRF2/NFE2L2 = nuclear factor erythroid 2-related factor 2; HIF1A = hypoxia inducible factor 1 subunit alpha)
Results show that NRF2 expression is regulated by NRG1 in papillary thyroid cancer (PTC).
27-OH induced autophagy is dependent on the relation between nuclear factor erythroid 2 p45-related factor 2 (Nrf2)-dependent antioxidant response and p62.
evidence for a direct role of NRF2 in globin gene regulation
the CD44-NRF2 axis might be a promising therapeutic target for the control of stress resistance and survival of CD44(high) CSC population within breast tumors.
this study shows changes of NRF2 expression levels induced by cell-free DNA in different cell types
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.
the KAT4 promoter was significantly activated by the transcriptional factors, NFE2related factor 2 and peroxisome proliferatoractivated receptor coactivator 1beta, which are targets of Syvn1induced degradation
By inhibiting binding of Keap1 to Nrf2.
Our data show reduced muscle mass and contractile force generation in old Nrf2-/- mice compared to age-matched wildtype mice associated with reduced mitochondrial oxygen consumption, increased mitochondrial ROS production, increased protein nitrosylation, cellular redox dysregulation, and reduced acetylcholine receptor expression.
Keap1-null mice showed that differentiation of both osteoclasts and osteoblasts was attenuated, showing that impaired differentiation of osteoblasts rather than osteoclasts is responsible for bone hypoplasia caused by Nrf2 hyperactivation.
Involved in the Nrf2/HO-1 pathway.
these data suggest that alleviation of the sustained mitochondrial dysfunction and oxidative stress through co-modulation of NRF2 and PINK1 may be in charge of restoration of the cognitive impairments in a mouse model of high-LET carbon ion irradiation
Here, the authors demonstrate that Tim-3 inhibits macrophage phagocytosis of Listeria monocytogenes by inhibiting the nuclear erythroid 2-related factor 2 (Nrf2) signaling pathway and increases bacterial burden.
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