Anti-Mouse NFE2L1 (FLJ00380), Rabbit Polyclonal
- Known as:
- Antibody toMouse NFE2L1 (FLJ00380), Rabbit Polyclonal
- Catalog number:
- mfl0380
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Sceti
- Gene target:
- Anti-Mouse NFE2L1 (FLJ00380) Rabbit Polyclonal
Related genes to: Anti-Mouse NFE2L1 (FLJ00380), Rabbit Polyclonal
- 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
Related products to: Anti-Mouse NFE2L1 (FLJ00380), Rabbit Polyclonal
Related articles to: Anti-Mouse NFE2L1 (FLJ00380), Rabbit Polyclonal
- In our previous study, coxsackievirus and adenovirus receptor (CXADR), a tight junction-associated protein, was shown to play a critical role in maintaining gingival epithelial barrier function. Smoking is a well-established risk factor for periodontal disease; however, the effects of heated tobacco products on epithelial barrier function remain poorly understood. The present study investigated the effects of three heated tobacco product extracts (HTPE) on CXADR expression in human gingival epithelial cells. Exposure to the three HTPE significantly reduced CXADR expression, and functional analyses supported the involvement of nuclear factor erythroid 2-like 1 (NFE2L1), a CNC-bZIP transcription factor, in the three HTPE-induced CXADR downregulation in gingival epithelial cells. In a three-dimensional multilayered gingival epithelial tissue model, HTPE exposure increased permeability to 40 kDa dextran and lipopolysaccharide, whereas CXADR overexpression attenuated the three HTPE-induced increase in permeability to these substrates. These findings indicate that the three HTPE compromise gingival barrier integrity, with CXADR downregulation contributing to increased permeability to bacterial components. - Source: PubMed
Publication date: 2026/09/25
Yamaga ShunsukeTanigaki KeitaSakanaka AkitoAmano AtsuoMatsusaki MichiyaTakeuchi HirokiKuboniwa Masae - Genetic studies of serious mental illness (SMI, including schizophrenia and bipolar disorder) have implicated two classes of risk variant: common variants , each of small effect but collectively accounting for most population-level risk, and ultra-rare coding variants which confer large risk in a small number of individuals. Most such studies cannot directly assess the impact of specific variants on SMI, transdiagnostically, as the phenotypic information that they collect is focused on a single diagnosis. Here we report results of association analysis of predicted deleterious variants from exome sequencing of 21,958 cases (SMI and severe major depressive disorder) and 19,826 controls from the Mision Origen biobank in the Paisa genetic isolate of Colombia. We identified transdiagnostic associations to seven genes, three at an exome-wide and four at a false discovery rate significance threshold. Five of these genes have not previously been implicated in SMI ( , , , , and - ); for the first four of these the association is driven by variants enriched in the Paisa due to a founder effect, filling the gap between ultra-rare and common variants. The strongest association that we observe is to a frameshift variant (7:904169:T:TC) in that is genome-wide significant for SMI, schizophrenia, and bipolar disorder and increases risk for both diagnoses by more than threefold; it truncates , a brain-enriched Arf6 GTPase-activating/scaffolding protein that has been mechanistically linked to post-mitotic neuronal morphogenesis and regulation of dendritic differentiation . Variant carriers differ significantly from other SMI cases in Mision Origen for psychotic, manic, and cognitive item-level phenotypes assessed through analyses of electronic health records and displayed impaired executive function on neurocognitive testing. Variant carriers differ significantly from other SMI cases in Mision Origen for multiple item-level phenotypes (psychotic, manic, and cognitive) assigned through natural language processing of longitudinal electronic health records. Although the 7:904169:T:TC variant is not significantly associated with major depressive disorder, carriers compared to others with this diagnosis display a significant increase in symptoms typical of bipolar disorder. The variant's high allele frequency in Mision Origen (~0.4%) will enable population-level studies to stratify SMI based on causation and identify additional factors influencing risk and resilience. - Source: PubMed
Publication date: 2026/09/27
Gerdes GretaTozzo VeronicaService Susan KFrydman-Gani ClaraDiaz-Zuluaga Ana MValencia-Echeverry JohannaArias AlejandroBicks Lucy KRamirez-Diaz Ana MSealock Julia MLiao CalwingHowrigan Daniel PLiu ChristianaLopera-Maya Esteban APimplaskar AdityaDe la Hoz Juan FArango-Gómez Mario AArango-Restrepo CamilaArbelaez-Herrera Maria CCamacho-Gualteros KatherineCardona-Arango MateoCastaño-Ramirez MauricioCastañeda-Hoyos Jaime ACerrato FeleciaChapman Sinéad BFranco-Gómez Roby ELondoño-Martinez John DMazo-Morales John SMejía-Piedrahita Juan CMir EmaadMoore Tyler MPerez-Jaramillo Luz EPérez-Vallejo MariaPosada-Ricardo Maria ERiscanevo-Posada VladimirRestrepo-Osorio CamilaRestrepo-Osorio DanielaRuparel KoshaSánchez-Patiño DaniloTeshiba TerriValdez JonathanValencia-Londoño WendyValencia-Zuluaga Oscar AVelez-Arango Jorge MCrossley Nicolas APalacio-Ortiz Juan DavidGeschwind Daniel HMartin Alicia RGur Ruben CSawaya Michael REisenberg David SEscobar Javier ISabatti ChiaraReus Victor IBearden Carrie ENeale Benjamin MLopez-Jaramillo CarlosFreimer Nelson BOlde Loohuis Loes - Sphingomyelin synthase 2 (SMS2) is a key enzyme in sphingomyelin synthesis and is implicated in atherosclerosis (AS). Both endothelial dysfunction (ED) and ferroptosis contribute to AS, but their relationship with SMS2 remains unclear. To explore this, we inhibited SMS2 with Ly93 and then performed RNA sequencing to assess its relationship with ferroptosis, as well as the expression, cholesterol homeostasis, and alternative splicing of NFE2L1 in endothelial cells. We also validated the relationship between SMS2, ferroptosis, and NFE2L1 in ApoE mice and clinical atherosclerotic plaque samples. Results showed that SMS2 inhibition by Ly93 reduced ferroptosis and ED. SMS2 inhibition also decreased cholesterol accumulation, enhanced skipping-exon (SE) alternative splicing of NFE2L1, and increased L-NFE2L1 levels; knockdown of L-NFE2L1 reversed these effects. In ApoE mice, endothelial-specific SMS2 overexpression worsened ED and plaque formation while reducing NFE2L1/GPX4 expression. Conversely, the ferroptosis inhibitor Fer-1 attenuated both ED and plaque burden. In unstable human plaques, SMS2 was elevated, whereas NFE2L1, GPX4, and SLC7A11 were reduced. Collectively, these findings suggest that SMS2 inhibition promotes L-NFE2L1 expression, and this effect is mediated, at least in part, by the suppression of cholesterol accumulation-driven alternative splicing of the NFE2L1 splicing event, a process that ultimately reduces oxidative stress. This depress ED via ferroptosis and ultimately decrease AS, identifying SMS2 as a potential therapeutic target. - Source: PubMed
Publication date: 2026/09/25
Zheng XimianWei YaoxinZhang TengXiong SimengXiong MingdiYang RenqiangYan Nianlong - Proteasome is an established therapeutic target in cancer, and proteasome inhibitors (PIs) such as bortezomib (BTZ) are clinically used for hematologic malignancies, including multiple myeloma. Although PIs have also been evaluated in solid tumors, their clinical efficacy has been limited. We therefore sought to develop a strategy to enhance PI efficacy using gemcitabine/cisplatin (GC)-resistant bladder cancer cells as a model of refractory solid cancer. One mechanism that limits PI efficacy is the nuclear factor erythroid 2-related factor 1 (NRF1, NFE2L1)-mediated proteasome bounce-back response, which restores proteasome capacity after inhibition. Because DNA damage-inducible 1 homolog 2 (DDI2)-mediated processing is required for NRF1 activation, we examined whether nelfinavir (NFV), a reported DDI2 inhibitor, could enhance BTZ sensitivity. GC-resistant T24GC cells exhibited increased basal proteasome activity, cross-resistance to PIs, and a stronger NRF1-mediated bounce-back response than parental T24 cells. NFV significantly enhanced BTZ-induced cytotoxicity and apoptosis in T24GC cells. Unexpectedly, NFV did not suppress the bounce-back response but instead further enhanced NRF1 activation in T24GC cells, possibly reflecting pharmacological actions of NFV beyond DDI2 inhibition. These findings identify enhanced NRF1-mediated proteasome adaptation as a feature of GC resistance and highlight the need for highly selective DDI2 inhibitors to evaluate DDI2-NRF1 targeting as a strategy to improve PI efficacy in drug-resistant solid cancers. - Source: PubMed
Publication date: 2026/09/23
Ota AtsumiKawai MinaHimura RinMaruyama SotaSaka TomofumiYoshino YutaYamada GokiTsujita TadayukiIkari AkiraEndo Satoshi - Cholesterol overload contributes to metabolic dysfunction-associated steatohepatitis (MASH) progression. One major pathway that limits hepatic cholesterol accumulation is export via VLDL secretion. While sterol regulatory element-binding protein (SREBP) activity is suppressed by insulin-induced gene 1 (INSIG1) under high sterol conditions, VLDL secretion nonetheless persists to prevent lipotoxicity and liver injury, presenting an unresolved paradox in cholesterol sensing and lipoprotein export. Here, we identified a cholesterol-responsive interaction between nuclear factor erythroid 2 related factor-1 (NFE2L1) and INSIG1 that preserved cholesterol homeostasis by sustaining VLDL secretion. Liver-specific NFE2L1 deletion elevated INSIG1 abundance, suppressed SREBP1 activation, and impaired VLDL secretion, leading to hepatic cholesterol accumulation and liver injury. Mechanistically, NFE2L1 bound to INSIG1 via its N-terminal homology box 2 (NHB2) domain; free cholesterol strengthened this interaction to promote INSIG1 degradation, thereby enabling SREBP1 activation and VLDL export. In NFE2L1-deficient mice, WT NFE2L1, but not a mutant NFE2L1 form unable to interact with INSIG1 (NHB2-deleted mutant, ΔNHB2), restored SREBP1 activity and VLDL secretion. Lipidomics analysis revealed that NFE2L1 deficiency reduced serum triglyceride composition, which was restored exclusively by WT NFE2L1. In a murine MASH model, NFE2L1 overexpression activated SREBP1/2, lowered hepatic cholesterol, and attenuated liver injury, inflammation, and fibrosis, without elevating atherogenic lipoproteins owing to compensatory LDL receptor upregulation. Together, these findings explain how VLDL secretion capacity was maintained under cholesterol excess and identify the NFE2L1/INSIG1 axis as a sterol-responsive safeguard for hepatic lipid homeostasis and a potential therapeutic target for MASH. - Source: PubMed
Publication date: 2026/07/15
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