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Validated All-in-One™ qPCR Primer for NFE2L2(NM_006164.4) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
NFE2 (MIM 601490), NFE2L1 (MIM 163260), and NFE2L2 comprise a family of human genes encoding basic leucine zipper (bZIP) transcription factors. They share highly conserved regions that are distinct from other bZIP families, such as JUN (MIM 165160) and FOS (MIM 164810), although remaining regions have diverged considerably from each other (Chan et al., 1995 [PubMed 7868116]).[supplied by OMIM].
Gene References into function
- Nrf2 is involved in antioxidant response element mediated transcriptional activation in response to acrolein exposure
- Nfe2l2 is involved in the regulation of Ucp1 by cAMP-mediated signaling.
- Keap1 dimerization causes Nrf2 sequestration
- expression inhibited laminar flow-induced NQO1 promoter activation in endothelial cells
- Nrf2 is required for the induction of ferritin in response to polycyclic aromatic xenobiotics and chemopreventive agents and may also play a role in basal transcription of both ferritin H and L
- Nrf2 is degraded by the ubiquitin-dependent pathway and phosphorylation of Nrf2 leads to an increase in its stability and subsequent transactivation activity
- phosphorylation of serine 40 is necessary for nuclear factor((erythroid-derived 2)like 2(Nrf2) release from Inhibitor of Nrf2(INrf2)
- This review describes the extensive analysis of the mechanisms involved in the stress response element (StRE)/Nrf2 transcription factor pathway for heme oxygenase-1 gene regulation.
- nf-e2 activated TXAS promoter in a dose-dependent manner.
- different segments of Nrf2 transactivation domain have different transactivation potential and different MAPKs have differential effects on Nrf2 transcriptional activity
- Data show that Keap1 associates with the N-terminal region of Cullin 3 through the IVR domain and promotes the ubiquitination of Nrf2 in cooperation with the Cullin 3-Roc1 complex.
- importance of examining the link between NRF2 polymorphisms and other oxidative stress-related diseases
- Nrf2 stabilization by pharmacological modulation or adenovirus-mediated Nrf2 overexpression might be viable strategies to prevent a wide-spectrum of oxidative stress-related neuronal cell injuries.
- Keap1 negatively regulates Nrf2 function in part by targeting Nrf2 for ubiquitination by the CUL3-ROC1 ligase and subsequent degradation by the proteasome
- Bach1 competes with Nrf2 leading to negative regulation of the antioxidant response element (ARE)-mediated NAD(P)H:quinone oxidoreductase 1 gene expression and induction in response to antioxidants
- analysis of Nrf2 nuclear import and export signals
- Nrf2 canonical nuclear export signal may help decipher the mechanisms governing nuclear localization and subsequent transcriptional activation of Nrf2-mediated cytoprotective genes.
- results suggest that pro-atherogenic oscillatory flow inhibits Nrf2 activity at the DNA binding step, thereby suppressing athero-protective gene expression and hence predisposing the blood vessels to the formation of atherosclerosis.
- Data suggest that some antioxidants may exert their anti-inflammatory and anticarcinogenic effects not only by induction of phase 2 enzymes but also by the up-regulation of the selenoprotein GI-GPx by Nrf2 binding.
- chlorogenic acid stimulates Nrf2, inhibits activator protein-1, NF-kappaB, and MAPKs and induces phase 2 detoxifying enzyme activity
- activation of PKC, p38(MAPK), JNK, ERK1/2, and Nrf2 by oxidized LDL in human smooth muscle cells leads to HO-1 induction, constituting an adaptive response against oxidative injury that can be ameliorated by vitamin C
- stabilization of Nrf2 in cells under stress represents the central regulatory response mediated by mechanisms that interfere with its interaction with Keap1, leading to the induction of antioxidant enzymes important to maintain cellular redox homeostasis
- Component of the c-Ha-ras ARE/EpRE heterocomplex. We conclude that both internal bases and flanking sequences regulate nuclear protein recruitment and complex assembly.
- nuclear factor-erythroid 2 p45-related factor 2 is a member of the Cap 'n' Collar family of transcription factors that binds to the antioxidant response elements
- alpha-lipoic acid induces HO-1 expression in THP-1 monocytic cells via Nrf2 and p38
- These findings suggest a role for FAC1 in apoptosis following release of Nrf2 from Keap1 in response to oxidative stress.
- Lipopolysaccharide induces heme oxygenase 1 mRNA and protein expression in monocytic cells via activation of the transcription factor Nrf2.
- Nrf2 expression significantly increases IL-8 mRNA levels and protein secretion in primary human kidney mesangial cells, aortic endothelial cells and malignant cell lines.
- p38 MAPK and Nrf2 have roles in phenolic acid-induced P-form phenol sulfotransferase expression in human hepatoma HepG2 cells
- These results suggest that the cytoprotective effect of deprenyl is, in part, dependent on Nrf2-mediated induction of antioxidative proteins, suggesting that activation of the PI3K-Nrf2 system may be a useful therapeutic strategy for PD.
- These data identify the Nrf2/ARE pathway as an endogenous atheroprotective system for antioxidant protection and suppression of redox-sensitive inflammatory genes.
- AKR1C1 promoter has an antioxidant response element which is bound by NRF2 in a ChiP analysis.
- a structural basis is provided for the loss of Keap1 function and gain of Nrf2 function in lung cancer cells
- Treatment of Hep-G2 cells with Nrf2-specific RNAi reduced Nrf2 & NQO2 gene expression & tBHQ induction. Nrf2 associates with JunD, binds to ARE at nucleotide -1433, & regulates human NQO2 gene expression & induction in response to antioxidants.
- Nrf2, through up-regulation of glutamate-cysteine ligase and increase of GSH levels, protects against CYP2E1-dependent AA toxicity
- GSK3beta inhibits the xenobiotic and antioxidant cell response by direct phosphorylation and nuclear exclusion of the transcription factor Nrf2
- This study thus manifests that a clear set of rules pertaining to the cis-acting element determine whether a given Maf-recognition elements preferentially associates with MafG homodimer or with MafG:Nrf2 heterodimer.
- Nrf2 may be self-sufficient to sense and transduce oxidative signals into the nucleus, consequently initiating antioxidant gene transcription
- Data demonstrate that induction of NADPH-dependent quinone oxidoreductase (Aor) activity by 15-Deoxy-Delta12,14-prostaglandin J2 is markedly attenuated in mouse embryonic fibroblasts that overexpress rat Aor.
- These results thus demonstrate that BRG1, through the facilitation of Z-DNA formation and subsequent recruitment of RNA polymerase II, is critical in Nrf2-mediated inducible expression of HO-1.
- Nrf2-mediated heme oxygenase-1 overexpression confers resistance to apoptosis induction by EGCG
- Ultraviolet b enhances nuclear export of Nrf1 and down regulates antioxidant response element mediated chemoprotective gene expression.
- Loss of KEAP1 function leading to constitutive activation of NRF2-mediated gene expression in cancer suggests that tumor cells manipulate the NRF2 pathway for their survival against chemotherapeutic agents
- The effect of Bach1 and Nrf2 on heme oxygenase 1 expression via cobalt protoporphyrin in human liver cells is reported.
- Endogenous transcripts of antioxidant genes NAD(P)H quinone oxidoreductase (NQO) 1 (NQO1) and glutathione S-transferase (GST) alpha1 accumulate as a consequence of Nrf2 overexpression.
- Activation of insulin signaling through PI3K/Akt/mTOR/Nrf2/ GCLc pathway affords significant cell protection by maintaining cellular redox balance.
- review will discuss recent progress in the field of the Nrf2-Keap1 signaling pathway, with emphasis on the mechanistic studies of Nrf2 regulation by Keap1--{REVIEW}
- The human prx1 promoter was cloned and nuclear factor (erythroid-derived 2)-related factor 2 (Nrf2) was identified as a key transcription factor.
- Nrf2-Keap1-dependent UGT1A1 induction by prooxidants might represent a key adaptive response to cellular oxidative stress
- NRF2 is a candidate susceptibility gene for risk of development of acute lung injury. Patients with the -617 A SNP had a significantly higher risk for developing ALI after major trauma.
- research of Nrf2 has opened up new opportunities in understanding how antioxidant defense pathways are regulated--REVIEW
- In 84 Japanese type 2 diabetes subjects, 14 genetic variations were found in the Nrf2 gene, including 9 novel ones.
- peroxiredoxin 1, but not NF-E2-related factor 2, has a role in non-small cell lung cancer recurrence and progression
- p65Nrf1 has the potential to play an important role in modulating the response to oxidative stress by functioning as a transdominant repressor of Nrf2-mediated activation of ARE-dependent gene transcription
- KEAP1 controls postinduction repression of the NRF2-mediated antioxidant response by escorting nuclear export of NRF2.
- Alterations in redox homeostasis are primarily the result of the phosphoinositol 3-kinase/Akt-dependent activation of Nrf2 and its downstream transcriptional targets.
- potentially higher levels of iron-generated oxidative stress related gene alleles may be at increased risk of breast cancer
- Preclinical evaluation of targeting the NRF2 pathway by CDDO-Im and CDDO-me for protection from LPS-induced inflammatory response and reactive oxygen species in peripheral blood mononuclear cells and neutrophils.
- the differential DNA binding specificity between Maf homodimers and Nrf2-Maf heterodimers establishes the differential gene regulation by these dimer-forming transcription factors
- NRP/B enhances oxidative stress responses in breast cancer cells via the Nrf2 pathway, identifying a novel role of nuclear matrix protein(s) in oxidative stress responses.
- Nrf2 regulates INrf2 by controlling its transcription, and INrf2 controls Nrf2 by degrading it.
- Results suggest that promoter polymorphisms of the Nrf2 gene are associated with the susceptibility to gastric ulcer.
- The Nrf2 pathway, which plays a protective role in normal cells, can be a potential target to control cancer cell cisplatin resistance.
- induction of ABCC2 and ABCG2 by tBHQ is mediated by the Nrf2/Keap1 system, whereas the induction of ABCC1 may involve a Keap1-dependent but Nrf2-independent mechanism.
- Livers from older donors have lower levels of Nrf2 perhaps exposing these organs to increrased ischemia-reperfusion injury.
- Fruit and vegetable consumption did not protect smokers from adenomas and did not interact with the NFE2L2 polymorphisms. The observed gene-gene interactions may point to a role for NFE2L2 polymorphisms in NQO1-related adenoma formation.
- the promoter polymorphisms of Nrf2 gene may affect the methylation status of tumor-related genes, especially the p14 gene, under the influence of H. pylori-induced gastric inflammation.
- Although epidermal growth factor receptor-MAPK pathway was highly activated by HOCl, it was not involved in Nrf2 activation and Nrf2-dependent gene expression. we conclude that Nrf2 directly protects airway epithelial cells from HOCl-induced toxicity.
- resveratrol attenuates cigarette-smoke extract(CSE)-mediated GSH depletion by inducing GSH synthesis and protects epithelial cells by reversing CSE-induced posttranslational modifications of Nrf2.
- cellular heme level plays an important role in determining the sensitivity of cells to imatinib and certain other anti-leukemia drugs and the effect of heme may be mediated via its ability to upregulate Nrf2 activity.
- a novel mechanism by which TNF-induced cell death is inhibited in AML cells through the induction of HO-1, via Nrf2 activation.
- importins alpha5 and beta1 associate with Nrf2, an interaction that was blocked by the nuclear import inhibitor SN50
- ProTalpha and Nrf2 compete for interaction with Keap1, therefore ProTalpha is able to liberate Nrf2 from complex with Keap1 and hence contribute to Nrf2-dependent transcription.
- We observed the nuclear translocation of the transcription factor Nrf2 associated with thinning of the actin stress fibers.
- Keap1 prevents activation of Nrf2 and lung cancer cell growth
- Examined the role of the Nrf2 pathway in regulating phase 2 metabolic genes in melanocytes and keratinocytes.
- the disruption of the Nrf2-antioxidant axis leads to increased oxidative stress and DNA damage in the initiation of cellular transformation in the prostate gland
- chlorophyllin exerts antioxidant effect by inducing HO-1 and NQO1 expression mediated by PI3K/Akt and Nrf2
- In this study, we demonstrate the dark side of Nrf2: stable overexpression of Nrf2 resulted in enhanced resistance of cancer cells to chemotherapeutic agents
- EGCG induces the expression of some antioxidant enzymes.
- stress-induced dephosphorylation of tyrosine 141 is a novel mechanism in Nrf2 activation and cellular protection
- KLF2 substantially enhances antioxidant activity of Nrf2 by increasing its nuclear localization and activation.
- Polymorphism of the Nrf2 gene promoter at -650C/A was associated with the development of vitiligo and A(-650) allele may be one of the risk factors.
- the COPD patient lungs showed significant decrease in NRF2 protein with decrease in NRF2-dependent antioxidants
- Cigarette smoke induces Nrf2 activation in macrophages, and Nrf2 expression is decreased in the macrophages of older current smokers and patients with chronic obstructive pulmonary disease.
- the anti-carcinogenic and antioxidant functions of lycopene may be mediated by apo-10'-lycopenoids via activating Nrf2 and inducing phase II detoxifying/antioxidant enzymes.
- constitutive Nrf2 activation may be involved in arsenic carcinogenesis of skin
- MafG-mediated nuclear retention may enable Nrf2 proteins to evade cytosolic proteasomal degradation and consequently stabilize Nrf2 signaling
- The -686*-684 genotype of Nrf2 gene may be associated with the development of ulcerative colitis.
- Nrf2 gene may be associated with the development of gastric inflammation and with gastric carcinogenesis
- UGT2B7 is transcriptionally regulated by Nrf2, but the mechanism is hindered by polymorphisms in the promoter region of UGT2B7*2.
- Aberrant Nrf2 activation provoked by Keap1 alteration is one of the molecular mechanisms for chemotherapeutic resistance in gallbladder cancer
- provides in vivo validation of the two-site substrate recognition model for Nrf2 activation by the Keap1-Cul3-based E3 ligase
- Reactive oxygen species-dependent Nrf2 activation plays an important role in lipoteichoic acid-mediated heme oxygenase-1 up-regulation in cultured human tracheal smooth muscle cells.
- alpha-lipoic acid controls cellular redox status, and upregulates quinone reductase NQO1 via Nrf2 activation in human leukemia HL-60 cells
- Targeting Nrf2 activity in lung cancers, particularly those with Keap1 mutations, could be a promising strategy to inhibit tumor growth and circumvent chemoresistance.
- This review is primarily focused on the role of Nrf2 in cancer, with emphasis on the recent findings indicating the its cancer promoting function--{REVIEW}
- Results suggest that a paradoxical decrease in Nrf-2 driven antioxidant responses in cystic fibrosis epithelia results in an increase in steady state H2O2, which in turn contributes to the overproduction of the pro-inflammatory cytokines IL-6 and IL-8.
- LPS induces NQO1 and HO-1 expression in human monocytes via Nrf2 to modulate their inflammatory responsiveness
- Resveratrol can prevent breast cancer initiation by blocking multiple sites in the estrogen genotoxicity pathway.
