Browse our anti-NRF2 (NFE2L2) Antibodies

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

1. Nrf2a-deficient zebrafish showed higher susceptibility to oxidative stress, and higher vulnerability to acetaminophen- or doxorubicin-induced toxicity.

2. 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.

3. Nrf2 was activated in response to the ER stress via the PERK pathway.

4. 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.

5. nrf2a modulates the embryonic response to perfluorooctanesulfonic acid (PFOS), and that PPAR signaling may play a role in the embryonic adaptive response to PFOS.

6. 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.

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

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

9. Coptisine exerted its antioxidant activity against AAPH-induced toxicity involving in activating Akt and JNK/Nrf2/NQO1 pathway.

10. 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.

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

12. 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.

13. 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.

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

15. 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

16. Nrf2 is protective against PFOS-induced oxidative stress in zebrafish larvae.

17. 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

18. 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

19. 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

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

1. this study highlighted the involvement of miR-153, miR-28 and miR-708 in regulatory network of Nrf2 mediated antioxidant system in bovine granulosa cells function.

2. 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.

3. 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.

4. expression of target genes in liver in transition period and stages of lactation

5. 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

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

1. 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.

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

3. 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. combination antiretroviral therapy increased monocyte/macrophage sensitivity to reactive oxygen species- in HIV(+) individuals by suppressing NRF2-ARE activity via p90RSK-mediated ERK5 S496 phosphorylation, which coordinately elicited senescent phenotypes and proinflammatory responses.

2. BRAF inhibitor-resistant melanoma exhibits a strong activation of NRF-2 pathway leading to increase in the pentose phosphate pathway.

3. Data show that NRF2 acting as a central node in the maintenance of low ROS levels and stemness associated properties of the CICs, which is significantly associated with the clinical outcome, but independent from ROS stress.

4. KEAP1- and NFE2L2-mutated NSCLC patients represent a highly heterogeneous patient cohort. Both are associated with different histologies and usually are found together with other cancer-related, partly targetable, genetic aberrations.

5. These data demonstrate that GR protects human melanocytes from H2O2induced oxidative damage via the Nrf2dependent induction of HO1, providing evidence for the application of GR in the treatment of vitiligo.

6. Our results suggest that GSTM1 * 1/0 genotype and the cumulative presence of at least one allele mutated in KEAP1 and/or NRF2 polymorphisms might be associated with worse prognosis for breast cancer patients.

7. The illustrate the elegant mechanisms used by these components to provide an immediate response, including NFE2L2 plasticity controlled by redox-sensing cysteines and the recruitment of naive proteins to the redox homeostasis array that act as chaperons in an ATP-independent manner.

8. This is the first study that has described the effects of KEAP1 silencing on the regulation of NRF2 activity in lung carcinoids cells. The epigenetic deregulation of the KEAP1/NRF2 by a KEAP1 promoter hypermethylation system appears to be a frequent event in lung carcinoids.

9. Sesn2 promoted the transfer of nuclear factor E2 related factor 2 to the cytoplasm, it decreased the expressions of Nrf2 and its downstream proteins, sulfiredoxin1 and thioredoxin1

10. Treatment with genistein significantly improved the altered cardiac function markers and oxidative stress markers. Genistein enhanced the Nrf2 and HO-1 expression, which showed protection against oxidative insult induced by doxorubicin.

11. These data demonstrated that external stimuli (eg, oxidative stress) may trigger autocrine HMGB1 translocation and release by melanocytes, suppressing the expression of Nrf2 and downstream antioxidant genes to induce melanocyte apoptosis, and thereby participate in the pathological process of vitiligo.

12. Nrf2 prevents inflammation caused by layer house PM2.5 stimulation, however, autophagy exerts a promotive role in TLR4 - NFkappaB p65 mediating inflammation in A549cell.

13. The HBXIP-mediated reduction in NRF2-KEAP1 complexes promotes NRF2 accumulation.

14. basal and inducible regulation of LAMP2A, and consequently Chaperone-mediated autophagy activity, by NFE2L2, is reported.

15. The Nrf2 is involved in other cellular processes, such as autophagy, intermediary metabolism, stem cell quiescence, and unfolded protein response.

16. The NRF2 plays during inflammation, the relationship between NRF2 and other transcription factors and mediators of inflammation still remains ambiguous.

17. The NRF2-KEAP1 signaling pathway is altered in cancer, how NRF2 is regulated by changes in cellular metabolism, and how NRF2 reprograms cellular metabolism to support proliferation.

18. The NRF2 activation and alterations to iron signaling in cancers may hinder efforts to induce the iron-dependent cell death process known as ferroptosis.

19. Nrf2-mediated metabolic reprogramming of tolerogenic dendritic cells is protective against aplastic anemia.

20. TRIM16 activates ubiquitin pathway genes and p62 via NRF2, leading to ubiquitination of misfolded proteins and formation of protein aggregates.

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

1. the results of this study suggest that DMHM inhibited several inflammatory pathways including the NF-kappaB and MAPK pathways, and induced Nrf2-mediated HO-1 expression, demonstrating its potential usefulness for treating inflammatory and neuroinflammatory diseases.

2. SIRT6 promotes transcription of a subset of NRF2 targets by mono-ADP-ribosylating BAF170.

3. Activation of the Nrf2 pathway is an effective means to profoundly ameliorate insulin resistance and completely prevent fatty liver and dyslipidemia in a mouse model. Importantly, Nrf2 activation almost doubles the age of the occurrence of sarcomas in this model, highlighting not only the efficiency of Nrf2 signaling in cancer, but also associating the ameliorated metabolic profile with delay in cancer progression.

4. combination antiretroviral therapy increased monocyte/macrophage sensitivity to reactive oxygen species- in HIV(+) individuals by suppressing NRF2-ARE activity via p90RSK-mediated ERK5 S496 phosphorylation, which coordinately elicited senescent phenotypes and proinflammatory responses

5. These findings suggest an essential role of the CX3CR1/NRF2 axis in microglial function and in tauopathies. Therefore, polymorphisms with loss of function in CX3CR1 or NRF2 have to be taken into account for the development of therapeutic strategies.

6. The present study reports the beneficial effects of SRT2104 on Diabetic nephropathy (DN), uncovering a SIRT1/P53/NRF2 pathway that modulates the pathogenesis of DN.

7. The present study explored the role of endothelin-1, H2S, and Nrf2 in remote preconditioning (RIPC)-induced beneficial effects in ischemia-reperfusion (I/R)-induced vascular dementia.

8. Sirt1-Nrf2-Cyclin B1 signaling pathway is important for regulating oocyte meiosis and aging.

9. The Nrf2 is an important regulator of the allergic response by determining the survival and death of ILC2s, and these findings suggest that Nrf2 activation is a potential therapeutic strategy for steroid-resistant allergy alleviation.

10. NRF2 may be implicated in memory and activity functions and its deletion exacerbates deficits associated with aging.

11. DUSP14 up-regulation inhibits inflammation and oxidative stress in brain of cerebral ischemia/reperfusion mice. DUSP14 evokes Nrf-2-meditated anti-oxidative stress and inflammatory response.

12. Mice deficient in IL-17D or the transcription factor Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), an inducer of IL-17D, featured an early decreased number of innate immune cells at the point of viral entry and were more susceptible to mouse cytomegalovirus infection.

13. data point to transcription factor NRF2 as a major mediator of oxidized palmitoyl-arachidonoyl-phosphatidylcholine -induced upregulation of SCF. This mechanism may represent one of the facets of pleiotropic action of NRF2 in vascular wall.

14. basal and inducible regulation of LAMP2A, and consequently Chaperone-mediated autophagy activity, by NFE2L2, is reported.

15. results confirmed a protective role for Nrf2 in late-stage carcinogenesis and, unexpectedly, suggest that activation of Nrf2 in immune cells may be advantageous for preventing or treating lung cancer

16. DC32 significantly suppressed rheumatoid arthritis (RA) via the Nrf2-p62-Keap1 feedback loop.

17. Nrf2-mediated metabolic reprogramming of tolerogenic dendritic cells is protective against aplastic anemia.

18. Oxidative Stress Induces an Interactive Decline in Wnt and Nrf2 Signaling in Degenerating Retinal Pigment Epithelium

19. The results from the in vivo study showed that bixin treatment attenuated the accumulation of inflammatory cells, decreased the levels of tissue apoptosis, and increase the ability of cell proliferation. Besides that, bixin also could regulate the expression of MMP9, TGFbeta1, and its downstream Fibronectin (FN), along with activation of Nrf2 signals

20. In mice, activation of the Nrf2 and SIRT1 signaling pathways ameliorated oxidative stress and mitochondrial dysfunction. Pharmacological targeting of Nrf2 signaling molecules may reduce the pathologic changes of aging in the kidney.