Ask about this productRelated genes to: NRBF2 antibody
- Gene:
- NRBF2 NIH gene
- Name:
- nuclear receptor binding factor 2
- Previous symbol:
- -
- Synonyms:
- DKFZp564C1664, FLJ30395, COPR1, COPR2
- Chromosome:
- 10q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-10
- Date modifiied:
- 2016-10-05
Related products to: NRBF2 antibody
Related articles to: NRBF2 antibody
- Arsenic exposure remains a leading environmental health concern. MicroRNA (miRNA) dysregulation may provide a mechanistic link to arsenic-related diseases, yet the associations of arsenic species and arsenic methylation capacity with miRNA profiles in plasma and leukocytes remain largely unexplored. In a community-based population of 160 Chinese adults, we characterized the miRNA signatures of urinary arsenic species [arsenate, As(V); arsenite, As(III); monomethylarsonate, MMA; dimethylarsinate, DMA], their summed concentration (ƩAs), and arsenic methylation capacity. We further explored their potential origins, target genes, and functional pathways using RNA-seq data and public databases. After adjusting for multiple comparisons (FDR < 0.15), we identified 80 plasma miRNAs and 9 leukocyte miRNAs associated with As(V), 2 leukocyte miRNAs associated with inorganic arsenic [iAs = As(V) + As(III)], 6 plasma miRNAs associated with MMA, and 2 plasma miRNAs associated with secondary methylation index (SMI = DMA/MMA). Notably, 65 % (52/80) of the As(V)-related plasma miRNAs were located in chromosome 14q32. Most of these identified plasma miRNAs showed high enrichment in lymphocytes and arsenic-target organs, such as adrenal gland and brain. In miRNA-mRNA co-expression analysis, the identified miRNAs primarily targeted NRBF2, NUP50, OSBPL11, and SIRPD, and may be involved in pathways related to cancer, inflammation and immune function, and oxidative stress. Our findings provided novel insights into the miRNA regulatory mechanisms involved in arsenic exposure response at low to moderate levels. - Source: PubMed
Publication date: 2025/12/22
Wang YaxinLi WendingLi WeiyaWang YufeiXu XuedanYuan RuochenZhang XiaoQu JingliLong PinpinWang HaoHe MeianZhang XiaominWu TangchunYuan Yu - The mammalian class III phosphatidylinositol-3-kinase complex (PtdIns3K) forms two biochemically and functionally distinct subcomplexes including the ATG14-containing complex I (PtdIns3K-C1) and the UVRAG-containing complex II (PtdIns3K-C2). Both subcomplexes adopt a V-shaped architecture with a BECN1-ATG14 or UVRAG adaptor arm and a PIK3R4/VPS15-PIK3C3/VPS34 catalytic arm. NRBF2 is a pro-autophagic modulator that specifically associates with PtdIns3K-C1 to enhance its kinase activity and promotes macroautophagy/autophagy. How NRBF2 exerts such a positive effect is not fully understood. Here we report that NRBF2 binds to PIK3R4/VPS15 with moderate affinity through a conserved site on its N-terminal MIT domain. The NRBF2-PIK3R4/VPS15 interaction is incompatible with the UVRAG-containing PtdIns3K-C2 because the C2 domain of UVRAG outcompetes NRBF2 for PIK3R4/VPS15 binding. Our crystal structure of the NRBF2 coiled-coil (CC) domain reveals a symmetric homodimer with multiple hydrophobic pairings at the CC interface, which is in distinct contrast to the asymmetric dimer observed in the yeast ortholog Atg38. Mutations in the CC domain that rendered NRBF2 monomeric led to weakened binding to PIK3R4/VPS15 and only partial rescue of autophagy deficiency in knockout cells. In comparison, NRBF2 with its CC domain replaced by a dimeric Gcn4 module showed proautophagic activity comparable to wild type while NRBF2 carrying a tetrameric Gcn4 module showed further enhanced activity. We propose that the oligomeric state of NRBF2 mediated by its CC domain is critical for strengthening the moderate NRBF2-PIK3R4/VPS15 interaction mediated by its MIT domain to fully activate PtdIns3K-C1 and promote autophagy. ATG: autophagy related; ATG14: autophagy related 14; BECN1: beclin 1; CC: coiled-coil; dCCD: delete CCD; dMIT: delete MIT; Gcn4: general control nonderepressible 4; ITC: isothermal titration calorimetry; IP: immunoprecipitation; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MIM: MIT-interacting motif; MIT: microtubule interacting and trafficking; NMR: nuclear magnetic resonance; NRBF2: nuclear receptor binding factor 2; PtdIns3K: class III phosphatidylinositol 3-kinase; PtdIns3P: phosphatidylinositol-3-phosphate; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PIK3R4/VPS15: phosphoinositide-3-kinase regulatory subunit 4; SQSTM1/p62: sequestosome 1; UVRAG: UV radiation resistance associated; VPS: vacuolar protein sorting; WT: wild type. - Source: PubMed
Publication date: 2025/11/12
Li NaLi XiaohuaQiu XianxiuPan XuehuaWu ShuaiChen JingyiLiu RongLu JiahongYue ZhenyuZhao Yanxiang - Large-scale kidney transcriptomics identifies a 12-gene signature, including and , predicting kidney failure in ANCA-associated vasculitis. This molecular signature outperformed Berden, renal risk score, and ANCA kidney risk score clinicopathologic classifications. ANCA-associated vasculitis with GN kidneys show broad immune dysregulation, notably in complement, TGF, and immunometabolism pathways. - Source: PubMed
Publication date: 2025/07/09
Brilland BenoîtRiou JérémieQuéméneur ThomasVandenbussche CyrilleMerillon NathalieBoizard-Moracchini AndreaRoy MaëvaDespré MaïaPiccoli Giorgina BarbaraDjema AssiaHenry NicolasPreisser LaurenceBlanchet OdileGnemmi VivianeCopin Marie-ChristineLanglais DavidJeannin PascaleBlanco PatrickDelneste YvesAugusto Jean-François - Selective clearance of damaged mitochondria through mitophagy is crucial for the maintenance of mitochondrial homeostasis. While mitophagy can be activated by various mitochondrial toxins, the physiologically relevant signal that triggers mitophagy is less studied. TGFB/TGFβ signaling has been linked to autophagic induction, but its specific role in mitophagy is not well understood. Here, we discovered a novel mitophagy induction paradigm stimulated by TGFB1. The mitophagic response is exclusively mediated by SMAD2, SMAD3, and SMAD4 underlying the TGFB receptor signaling. The transcriptional regulation activates genes involved in the canonical autophagic pathway which is required for the TGFB1-induced mitophagy. Moreover, TGFB1 signaling promotes mitophagic flux by upregulating PLSCR3 that externalizes cardiolipin in conjunction with the MAP1LC3/LC3/GABARAPs-interacting receptor proteins (BNIP3L/NIX, BNIP3, and FUNDC1)-dependent mechanism. Overall, our study characterized the essential components engaged in the TGFB1-induced mitophagy and demonstrated that TGFB is an important signal that induces mitophagy. ATG5: autophagy related 5; ATG8: mammalian homolog of yeast Atg8; ATG9A: autophagy related 9A; ATG13: autophagy related 13; ATG101: autophagy related 101; BNIP3: BCL2 interacting protein 3; BNIP3L/NIX: BCL2 interacting protein 3 like; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; Cardiolipin: 1,3-bis(-3'-phosphatidyl)--glycerol; CERS1: ceramide synthase 1; FUNDC1: FUN14 domain containing 1; GABARAP: GABA type A receptor-associated protein; GABARAPL1: GABA type A receptor-associated protein like 1; GABARAPL2: GABA type A receptor-associated protein like 2; GLS: glutaminase; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MitoIP: mitochondrial immunoprecipitation; MMP: mitochondrial membrane potential; NRBF2: nuclear receptor binding factor 2; OPTN: optineurin; PINK1: PTEN induced kinase 1; PLSCR3: phospholipid scramblase 3; PRKN: parkin RBR E3 ubiquitin protein ligase; RB1CC1/FIP200: RB1 inducible coiled-coil 1; TGFB/TGFβ: transforming growth factor beta; ULK1: unc-51 like autophagy activating kinase 1. - Source: PubMed
Publication date: 2025/04/01
Yan JiongChen XinChoksi SwatiLiu Zheng-Gang - NRBF2, a component of autophagy-associated PIK3C3/VPS34-containing phosphatidylinositol 3-kinase complex, plays a crucial role in learning and memory processes, yet its specific impact on memory and the underlying molecular mechanisms remains unclear. - Source: PubMed
Publication date: 2025/02/12
Wu SongfenZhuang HaicaiZhou XidanLi Kuan