NFE2L1 polyclonal antibody (A01)
- Known as:
- NFE2L1 pab (anti-) (A01)
- Catalog number:
- H00004779-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- NFE2L1 polyclonal antibody (A01)
Related genes to: NFE2L1 polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: NFE2L1 polyclonal antibody (A01)
Related articles to: NFE2L1 polyclonal antibody (A01)
- Endometriosis (EMs) is a chronic inflammatory disease characterized by ectopic growth of endometrial-like tissues. N-methyladenosine (mA) modification regulates diverse cellular processes, yet its role in EMs remains unclear. Here, we show that the mA reader YTHDF2 is downregulated in ectopic tissue and endometrial stromal cells. Overexpression of YTHDF2 in HESCs suppresses proliferation and migration while promoting apoptosis, whereas its knockdown exerts opposite effects. In vivo, AAV9-mediated Ythdf2 delivery inhibits lesion growth, while inhibition of YTHDF2 accelerates disease progression. Mechanistically, hypoxia induces HDAC11 via HIF-1α, reducing acetylation of the YTHDF2 promoter and leading to transcriptional silencing. RNA-seq reveals that YTHDF2 loss activates NF-κB signaling. Integrative MeRIP-seq, RIP-seq, and scRNA-seq analyses identify NFE2L1 as a direct downstream target whose mRNA stability is enhanced upon YTHDF2 depletion in an mA-dependent manner. Elevated NFE2L1 activates STAT3 and CARD11, potent NF-κB inducers. Collectively, our study uncovers a mechanism whereby epigenetic silencing of YTHDF2 drives EMs progression through the NFE2L1-NF-κB axis, suggesting YTHDF2 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/05/19
Wang TaoPeng XiaotongYang PushengJi MeMiao YaxinZhang JiaxinLiu WenwenZhu YipingTang MingSun Jing - Migraine, a prevalent and debilitating neurovascular disorder, frequently co-occurs with functional dyspepsia. Emerging evidence suggests that infection may contribute to both conditions via neuroimmune pathways, though the molecular basis for this association has yet to be fully elucidated. - Source: PubMed
Publication date: 2026/04/28
Sun NengjinWang KaileGou JianliLi PanpanFu XiaoyanShi WenjingLi JingXiang MiaoSun ShenglinSun ZihanLiang ShujuanZhang YuyingWang Hongyan - 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 - Nfe2l1 is a transcription factor that is highly conserved and is encoded by the Nuclear Factor Erythroid 2 Like 1 (Nfe2l1) gene, which responds to oxidative stress, proteotoxic stress, and endoplasmic reticulum stress in cells; However, its specific role in the context of acute kidney injury (AKI) is not fully understood. - Source: PubMed
Publication date: 2026/05/03
Hu JianqiangZhang YueweiZhang YanZhang YanminCi Xinxin - Aortic valve disease (AVD) is a cardiovascular disorder highly prevalent in the elderly population. Aortic valve leaflets suffer hardening due to extracellular matrix (ECM) remodeling and subsequent calcification, leading to impaired blood flow and aortic valve stenosis. Valve interstitial cells (VICs) are fibroblast-like cells that can undergo myofibroblast activation and osteogenic transformation, contributing to disease progression. - Source: PubMed
Publication date: 2026/04/07
Macarie Răzvan DȚucureanu Monica MCiortan LetițiaPreda Mihai BogdanMânduțeanu IleanaButoi Elena