NRF2 EMSA Kit
- Known as:
- NRF2 EMSA Kit
- Catalog number:
- AY1225
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- NRF2 EMSA Kit
Related genes to: NRF2 EMSA Kit
- Gene:
- GABPA NIH gene
- Name:
- GA binding protein transcription factor subunit alpha
- Previous symbol:
- -
- Synonyms:
- E4TF1A, NFT2, NRF2, E4TF1-60, NRF2A
- Chromosome:
- 21q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-01-18
- Date modifiied:
- 2018-04-23
- Gene:
- NFE2L2 NIH gene
- Name:
- nuclear factor, erythroid 2 like 2
- Previous symbol:
- -
- Synonyms:
- NRF2
- Chromosome:
- 2q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-24
- Date modifiied:
- 2016-10-05
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- In recent years, the acronym NRF2 has garnered significant attention in scientific discourse. However, this attention has occasionally led to confusion due to the existence of two distinct proteins sharing the same acronym: Nuclear Respiratory Factor 2 (NRF2), also known as GA-binding protein transcription factor subunit alpha (GABPA), and Nuclear Factor Erythroid 2-related Factor 2 (NFE2L2 or NRF2). This confusion has been highlighted in various scientific forums, including PubPeer and anonymous reader comments, where the confusion between the two proteins has been expressed. In this article, we aim to elucidate the disparities between these two proteins. Both are transcription factors that play pivotal roles in cellular homeostasis and response to stress, with some overlapping functional aspects. Nuclear Factor Erythroid 2-related Factor 2 (NFE2L2) is a key regulator of the antioxidant response element (ARE) pathway. It functions by binding to antioxidant response elements in the promoters of target genes, thereby orchestrating the expression of various cytoprotective enzymes and proteins involved in detoxification, redox balance, and cellular defense against oxidative stress. Conversely, Nuclear Respiratory Factor 2 (GABPA) is primarily associated with the regulation of mitochondrial biogenesis, in relation to PGC1α, and maintaining cellular energy metabolism. It is important to recognize and differentiate between these two proteins to avoid misconceptions and misinterpretations in scientific literature and discussions. Our laboratories (Arubala P Reddy and P. Hemachandra Reddy) focued on Nuclear Respiratory Factor 2 (NRF2), but not on Nuclear Factor Erythroid 2-related Factor 2 (NFE2L2). We hope that the facts, figures, and discussions presented in this article will clarify the current controversy regarding the sizes, structural features, and functional aspects of these proteins. - Source: PubMed
Publication date: 2024/05/28
George MathewReddy Arubala PReddy P HemachandraKshirsagar Sudhir - Males are more susceptible to brain mitochondrial bioenergetic dysfunction following neonatal cerebral hypoxic-ischemia (HI) than females. Mitochondrial biogenesis has been implicated in the cellular response to HI injury, but sex differences in biogenesis following HI have not been described. We tested the hypothesis that mitochondrial biogenesis or the expression of mitochondrial electron transport chain (ETC) proteins are differentially stimulated in the brains of 8 day old male and female rats one day following HI, and promoted by treatment with acetyl-L-carnitine (ALCAR). There were no sex differences in mitochondrial mass, as reflected by the ratio of mitochondrial to nuclear DNA (mtDNA/nDNA) and citrate synthase enzyme activity present one day following HI or sham surgery. There was an increase in mtDNA/nDNA, however, in the hypoxic and ischemic (ipsilateral) hemisphere after HI in both male and female brains at one day post-injury, which was suppressed by ALCAR. Citrate synthase activity was increased in the ipsilateral hemisphere of ALCAR treated male and female brain. Most importantly, the levels of representative mitochondrial proteins present in ETC complexes I, II and IV increased substantially one day following HI in female, but not male brain. This sex difference is consistent with the increase in the mitochondrial biogenesis-associated transcription factor NRF-2/GABPα following HI in females, in contrast to the decrease observed with males. In conclusion, the female sex-selective increase in ETC proteins following HI may at least partially explain the relative female resilience to mitochondrial respiratory impairment and neuronal death that occur after HI. - Source: PubMed
Publication date: 2016/09/28
Demarest T GSchuh R AWaite E LWaddell JMcKenna M CFiskum Gary - The transcription factor nuclear factor-erythroid-derived 2-like 2 (official symbol: NFE2L2, alias: Nrf2) is a master regulator of antioxidant defense system, which makes it an attractive target for manipulations that aim to increase cellular resistance to oxidative stress. Nuclear respiratory factor 2 or GA binding protein transcription factor alpha (official symbol: GABPA, alias: NRF2) functions as a transcription factor that activates the expression of some key metabolic genes regulating cellular growth and nuclear genes required for mitochondrial respiration as well as mitochondrial DNA transcription and replication. - Source: PubMed
Publication date: 2013/04/15
Baldelli SaraAquilano KatiaCiriolo Maria R - The induction of heme oxygenase-1 (HO-1; Hmox1) by inflammation, for instance in sepsis, is associated both with an anti-inflammatory response and with mitochondrial biogenesis. Here, we tested the idea that HO-1, acting through the Nfe2l2 (Nrf2) transcription factor, links anti-inflammatory cytokine expression to activation of mitochondrial biogenesis. HO-1 induction after LPS stimulated anti-inflammatory IL-10 and IL-1 receptor antagonist (IL-1Ra) expression in mouse liver, human HepG2 cells, and mouse J774.1 macrophages but blunted tumor necrosis factor-α expression. This was accompanied by nuclear Nfe2l2 accumulation and led us to identify abundant Nfe2l2 and other mitochondrial biogenesis transcription factor binding sites in the promoter regions of IL10 and IL1Ra compared with pro-inflammatory genes regulated by NF-κΒ. Mechanistically, HO-1, through its CO product, enabled these transcription factors to bind the core IL10 and IL1Ra promoters, which for IL10 included Nfe2l2, nuclear respiratory factor (NRF)-2 (Gabpa), and MEF2, and for IL1Ra, included NRF-1 and MEF2. In cells, Hmox1 or Nfe2l2 RNA silencing prevented IL-10 and IL-1Ra up-regulation, and HO-1 induction failed post-LPS in Nfe2l2-silenced cells and post-sepsis in Nfe2l2(-/-) mice. Nfe2l2(-/-) mice compared with WT mice, showed more liver damage, higher mortality, and ineffective CO rescue in sepsis. Nfe2l2(-/-) mice in sepsis also generated higher hepatic TNF-α mRNA levels, lower NRF-1 and PGC-1α mRNA levels, and no enhancement of anti-inflammatory Il10, Socs3, or bcl-x(L) gene expression. These findings disclose a highly structured transcriptional network that couples mitochondrial biogenesis to counter-inflammation with major implications for immune suppression in sepsis. - Source: PubMed
Publication date: 2011/03/18
Piantadosi Claude AWithers Crystal MBartz Raquel RMacGarvey Nancy ChouFu PingSweeney Timothy EWelty-Wolf Karen ESuliman Hagir B