NRF1 EMSA Kit
- Known as:
- NRF1 EMSA Kit
- Catalog number:
- AY1224
- Product Quantity:
- 25 rxn
- Category:
- -
- Supplier:
- Panomics
- Gene target:
- NRF1 EMSA Kit
Related genes to: NRF1 EMSA Kit
- Gene:
- NFE2L1 NIH gene
- Name:
- nuclear factor, erythroid 2 like 1
- Previous symbol:
- TCF11
- Synonyms:
- NRF1, LCR-F1, FLJ00380
- Chromosome:
- 17q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-03-24
- Date modifiied:
- 2015-11-18
- Gene:
- NRF1 NIH gene
- Name:
- nuclear respiratory factor 1
- Previous symbol:
- -
- Synonyms:
- EWG, ALPHA-PAL
- Chromosome:
- 7q32.2
- Locus Type:
- gene with protein product
- Date approved:
- 1995-11-01
- Date modifiied:
- 2016-10-05
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- Nuclear factor erythroid 2-related factor 1 (Nrf1, encoded by NFE2L1) plays a central role in maintaining cellular homeostasis, basal redox balance, and mitochondrial quality control and its function. Recent studies have revealed that Nrf1 assumes complex, even opposing, roles in functioning both as a tumor-suppressor and otherwise, also as an unconvincing driver of Hepatocellular carcinoma (HCC) progression through certain oncogenic pathways and redox stress adaptation. - Source: PubMed
Publication date: 2026/06/29
Chen XiZhang ZhengwenCui SiqianZhang Yiguo - In diabetic nephropathy (DN), oxidative stress disrupts normal metabolic processes, contributing to progressive kidney injury. Although Nfe2l1 (also known as Nrf1) is known to regulate oxidative stress and metabolism, its specific role in DN remains poorly understood. This study investigated how changes in Nrf1 expression influence DN-associated renal fibrosis. - Source: PubMed
Publication date: 2026/06/12
Qiu ZiyingZhang YanminZhu LaiyuZhao XuanruiLi XinyaGong XiaokeCi Xinxin - Proteasome inhibitor drugs are currently used in the clinic to treat multiple myeloma and mantle cell lymphoma. These inhibitors cause accumulation of undegraded proteins, thus inducing proteotoxic stress and consequent cell death. However, cancer cells counteract this effect by activating an adaptive response through the transcription factor nuclear factor erythroid 2-related factor 1 (NRF1, also known as NFE2L1). NRF1 induces transcriptional upregulation of proteasome and autophagy/lysosomal genes, thereby reducing proteotoxic stress and diminishing the effectiveness of proteasome inhibition. While suppressing this protective autophagy response is one potential strategy, here we investigated whether this heightened autophagy could instead be leveraged therapeutically. To this end, we designed an autophagy-targeting chimera (AUTAC) compound to selectively degrade the anti-apoptotic protein Mcl1 via the lysosome. Our results show that this lysosome-mediated targeted degradation is significantly amplified in the presence of proteasome inhibition, in a NRF1-dependent manner. Mechanistically, AUTAC-driven Mcl1 clearance requires K63-linked ubiquitination by UBC13 and TRAF6 and recognition by the cargo receptor p62/SQSTM1. The combination of the proteasome inhibitor carfilzomib and Mcl1 AUTAC synergistically promoted cell death in both in vitro models, including wild-type and proteasome inhibitor-resistant multiple myeloma and lung cancer cells, and in mouse tumor xenografts. Thus, our work offers a novel strategy for enhancing proteasome inhibitor efficacy by exploiting the adaptive autophagy response. More broadly, our study establishes a framework for amplifying lysosome-mediated targeted protein degradation, with potential applications in cancer therapeutics and beyond. - Source: PubMed
Publication date: 2026/05/11
Elshazly Ahmed MHosseini NayyerehalsadatVangala JanakiramShen ShanweiNeely VictoriaHu XiaoyanPagare Piyusha PHarada HisashiGrant StevenRadhakrishnan Senthil K - Proteolytic stress frequently arises during disease and aging, particularly in long-lived, post-mitotic cells such as cardiomyocytes. To maintain proteostasis, cardiomyocytes depend on coordinated protein quality control pathways, including the ubiquitin-proteasome system and autophagy. Mechanisms that activate these pathways hold therapeutic potential for heart disease. Here, we demonstrate that transient activation of nuclear factor erythroid 2-like 1 (Nfe2l1, also known as Nrf1), a transcriptional regulator of proteasome activity, in cardiomyocytes during ischemia/reperfusion injury improves cardiac function. In addition to regulating the proteasome, we identify a critical role for Nrf1 in activating autophagy, which is essential for its cardioprotective effects. Through multi-omics analyses, we define both transcriptional and post-transcriptional functions of Nrf1 that underlie its cardioprotective activity. Loss-of-function studies in mice demonstrate that Nrf1, but not its homolog Nrf2, is required for autophagy and baseline cardiac function. Together, our findings establish a dual function of Nrf1 in promoting cardiac proteostasis by regulating both proteasomal and autophagic protein quality control pathways. Activating Nrf1 thus offers a therapeutic strategy for treating ischemic heart disease. - Source: PubMed
Publication date: 2026/04/17
Kankanamge Lakindu PAn HyunjiGuo QinProndzynski MaksymillianKwon Soon HoBonde Durgesh AnilPu William TOlson Eric NCui Miao - The proteasome is essential for cellular protein homeostasis through selective destruction of damaged and misfolded proteins. Failure of proteasome-dependent turnover accompanied by accumulation and aggregation of aberrant proteins is a hallmark of aging and late-onset neurodegenerative diseases. SKN-1A/Nrf1, a member of the NFE2L/Nrf family of transcription factors, is a master regulator of proteasome biogenesis. Through transcriptional control of proteasome subunit gene expression, SKN-1A/Nrf1 controls homoeostatic and stress-responsive upregulation of proteasome levels in adaptation to proteasome dysfunction or protein misfolding. SKN-1A/Nrf1 acts in concert with another Nrf family transcription factor, SKN-1C/Nrf2, to regulate many aspects of physiology including stress responses, redox balance, immunity, and metabolism. Here, we demonstrate that a small deletion in the promoter of the pbs-5 gene, which encodes an essential proteasome subunit, uncouples its expression from transcriptional regulation by SKN-1A/Nrf1. This disruption leads to compensatory SKN-1A/Nrf1-dependent upregulation of other proteasome subunit genes, resulting in a homeostatic imbalance in proteasomal gene expression. This pbs-5 regulatory mutation phenocopies some, but not all, aspects of SKN-1A/Nrf1 inactivation, providing evidence that coordinated regulation of proteasomal subunit gene expression underlies a subset of SKN-1A/Nrf1's physiological roles. In comparing the effects of the pbs-5 promoter deletion with isoform-specific inactivation of SKN-1A or SKN-1C, we show that the pbs-5 promoter mutation completely abrogates multiple lifespan extension paradigms. These results reveal that coordinated homeostatic regulation of proteasome subunit gene expression is critical for longevity and healthy aging. - Source: PubMed
Publication date: 2026/02/17
Topalidou IriniLehrbach Nicolas