Browse our anti-NRF2 (NFE2L2) Antibodies

Zebrafish Nuclear Factor (erythroid-Derived 2)-Like 2 (NFE2L2) interaction partners

1. These results suggest that alpha,beta-unsaturated carbonyl entity and catechol moiety of 6S derivatives may react with the cysteine residues of Keap1 (show KEAP1 Antibodies), disrupting the Keap1 (show KEAP1 Antibodies)-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.

2. These data suggest that EC from the Tripterygium wilfordii stem extract could diminish tau-GFP-induced neuronal death through the activation of Nrf2.

3. we concluded that Nrf2 plays a fundamental and conserved role in protection against acute sodium arsenite toxicity

4. Coptisine exerted its antioxidant activity against AAPH-induced toxicity involving in activating Akt (show AKT1 Antibodies) and JNK (show MAPK8 Antibodies)/Nrf2/NQO1 (show NQO1 Antibodies) pathway.

5. Bach1 (show BACH1 Antibodies) regulates the liver specificity and transience of the Nrf2a-dependent induction of hmox1a and that heme mediates this regulation through Bach1 (show BACH1 Antibodies) inhibition based on its level in each tissue.

6. The Bach1b-MafK heterodimer represses the zymogen promoters, whereas the Nrf2a-MafK heterodimer activates them.

7. 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.

8. 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.

9. results revealed that nrf2 mutant zebrafish are viable and fertile but show an increased susceptibility to oxidative stress and electrophiles

10. 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

Cow (Bovine) Nuclear Factor (erythroid-Derived 2)-Like 2 (NFE2L2) interaction partners

1. 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 (show HMOX1 Antibodies) within these cells.

2. 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.

3. investigation of molecular mechanisms of microvascular complications in diabetes/hyperglycemia: Nrf2 is involved in regulation of HO-1 (show HMOX1 Antibodies) gene expression in aortic endothelial cells by advanced glycation end products

Pig (Porcine) Nuclear Factor (erythroid-Derived 2)-Like 2 (NFE2L2) interaction partners

1. Lack of Nrf2 enhances susceptibility to mycotoxin-induced kidney disease.

2. 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.

Human Nuclear Factor (erythroid-Derived 2)-Like 2 (NFE2L2) interaction partners

1. The data identify an intricate mechanism of hepatitis C virus-dependent inhibition of Nrf2 (show GABPA Antibodies)/ antioxidant response elements-mediated gene expression which counteracts serine 349-phosphorylated p62 (show GTF2H1 Antibodies)-induced activation of Nrf2 (show GABPA Antibodies).

2. These results indicate that dual-negative expression of Nrf2 (show GABPA Antibodies) and NQO1 (show NQO1 Antibodies) is predictive of a better prognosis in NSCLC patients.

3. Besides being sensitivity to oxidative stress and therefore regulate the expression of detoxifying enzymes, Nrf2 (show GABPA Antibodies) can also regulate anti-inflammatory cellular responses, by inhibiting NF-kB in chronic kidney disease. [Review]

4. These results indicated that ROS (show ROS1 Antibodies)-induced BGN (show BGN Antibodies) caused the pro-angiogenic phenotype in TECs via NRF2 (show GABPA Antibodies) dysregulation.

5. Curcumin Protects Skin against UVB-Induced Cytotoxicity via the Keap1 (show KEAP1 Antibodies)-Nrf2 (show GABPA Antibodies) Pathway: The Use of a Microemulsion Delivery System.

6. The findings indicate that expression of the transcription factor NRF2 and its effector GCL are both profoundly deregulated in endometriotic lesions towards increased growth and fibrogenetic processes.

7. Results show that Nrf2 (show GABPA Antibodies) was down-regulated by cathepsin D (show CTSD Antibodies) knockdown. Importantly, Nrf2 (show GABPA Antibodies) overexpression significantly reduced cell senescence. Although transient oxidative stress promoted the accumulation of Nrf2 (show GABPA Antibodies) in the nucleus, Nrf2 (show GABPA Antibodies) protein exited nucleus if oxidative stress persisted in cancer cells.

8. It provides novel insights into Nrf2 (show GABPA Antibodies)-mediated of cell proliferation in non-small cell lung cancer (NSCLC) and may facilitate therapeutic development against NSCLC.

9. Dihydromyricetin (DMY) protects HUVECs from ox-LDL-induced oxidative injury by activating Akt (show AKT1 Antibodies) and ERK1/2, which subsequently activates Nrf2 (show GABPA Antibodies)/HO-1 (show HMOX1 Antibodies) signaling, thereby up-regulating antioxidant enzymes and anti-apoptotic proteins.

10. Results demonstrated that patients with NRF2 (show GABPA Antibodies) overexpression had poorer survival, irrespective of overall survival and disease free survival, compared to patients with low NRF2 (show GABPA Antibodies) expression. This data suggests that the biological behavior of tumors with NRF2 (show GABPA Antibodies) overexpression is more aggressive. [meta-analysis]

Mouse (Murine) Nuclear Factor (erythroid-Derived 2)-Like 2 (NFE2L2) interaction partners

1. baicalin enhanced NRF2 activation by nuclear translocation and induced its target genes HO-1 (show HMOX1 Antibodies) and GCLM (show GCLM Antibodies), thus enhancing antioxidant defense. Interplay of oxidative stress/inflammation and NRF2 were key players for baicalin-mediated protection.

2. the suppression of Nrf2 attenuates adipogenesis and decreases FGF21 (show FGF21 Antibodies) expression through PPARgamma (show PPARG Antibodies) in 3T3-L1 cells.

3. The findings indicate that expression of the transcription factor NRF2 and its effector GCL are both profoundly deregulated in endometriotic lesions towards increased growth and fibrogenetic processes.

4. the incidence, multiplicity and burden of Cutaneous squamous cell carcinomas that form in Keap1 (show KEAP1 Antibodies)(flox/flox)/Nrf2(-/-) mice are much greater than in their Keap1 (show KEAP1 Antibodies)(flox/flox)/Nrf2(+/+) counterparts, establishing Nrf2 activation as the protection mediator.

5. Dimethyl fumarate prevents diabetes-induced myocardial tissue injury, likely via activation of Nrf2 function.

6. Study emphasizes the critical role of Nrf2 in maintaining healthy cerebrovascular conditions and blood-brain barrier endothelial structure and functional integrity. Data suggests that cigarette smoke significantly impairs the cerebrovascular condition and endothelial function by increased load of oxidative stress due to altered Nrf2 signaling.

7. Data show that Nrf2is the master regulator of cellular redox homeostasis and its activation leads to a reductive-state in the myocardium. The transgene dose dependent expression of constitutively active Nrf2 is sufficient to develop a "pro-reductive" stable redox state that is not compensated for by modification of other signaling pathways or proteins associated with antioxidant response element (ARE) transcription.

8. The results demonstrated that restoration of Brg1 (show SMARCA4 Antibodies) during reperfusion could enhance Nrf2-mediated inducible expression of HO-1 (show HMOX1 Antibodies) during hepatic ischemia-reperfusion injury to effectively increase antioxidant ability to combat against hepatocytes damage.

9. The in vitro study illustrated that the anti-inflammatory effects of RA-XII were partially reversed following Nrf2 and HO-1 (show HMOX1 Antibodies) inhibition. Together, these findings strongly suggested that RA-XII is a potential agent against acute kidney injury.

10. It is a key transcription factor regulating HO-1 (show HMOX1 Antibodies) induction.