FNIP1 folliculin interacting protein 1 antibody
- Known as:
- FNIP1 folliculin interacting protein 1 (anti-)
- Catalog number:
- orb76627
- Product Quantity:
- 50 ul
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FNIP1 folliculin interacting protein 1 antibody
Ask about this productRelated genes to: FNIP1 folliculin interacting protein 1 antibody
- Gene:
- FNIP1 NIH gene
- Name:
- folliculin interacting protein 1
- Previous symbol:
- -
- Synonyms:
- KIAA1961
- Chromosome:
- 5q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2005-08-09
- Date modifiied:
- 2016-10-05
Related products to: FNIP1 folliculin interacting protein 1 antibody
Related articles to: FNIP1 folliculin interacting protein 1 antibody
- Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading cause of chronic liver disease. MTOR (mechanistic target of rapamycin kinase) complex 1 (MTORC1) is a potential therapeutic target, whereas suppression of total MTORC1 activity can lead to unwanted effects. Here, we found that byakangelicin (Bya), a natural compound, selectively inhibited MTORC1-mediated phosphorylation of TFEB (transcription factor EB), without affecting canonical MTORC1 substrates. Knockout of hepatic blocked the alleviation effects of Bya on hepatic steatosis, inflammation, insulin resistance, and fibrosis in mice, while reintroduction of TFEB restored these effects. We identified Bya directly bound to MET370 and PHE552 of FLCN (folliculin), suppressing the function of the FLCN-FNIP1 (folliculin interacting protein 1)/FNIP2 complex, which in turn inhibited MTORC1-mediated cytoplasmic sequestration of TFEB. Mutation of FLCN (M370A and F552A) in the liver abolished Bya-induced protection against MASH. Thus, Bya is a promising therapeutic natural compound for MASH, and selective inhibition of MTORC1 is a potential approach to treat this disease. aa, amino acids; AAV, adeno-associated virus; Bio, biotin; Bio-Bya, biotin-conjugated Bya; BSA, bovine serum albumin; BW, body weight; Bya, byakangelicin; CETSA, cellular thermal shift assay; CHIP-atlas, chromatin immunoprecipitation atlas; C, maximum concentration; CQ, chloroquine; DARTS; drug affinity responsive target stability assay; EIF4EBP1/4E-BP1, eukaryotic translation initiation factor 4E binding protein 1; FBS, fetal bovine serum; FDA, food and drug administration; FIMO-JASPAR, find individual motif occurrences-JASPAR; FLCN, folliculin; FNIP1, folliculin interacting protein 1; GAP, GTPase-activating protein; GOT1/AST, glutamic-oxaloacetic transaminase 1; GPT/ALT, glutamic-pyruvic transaminase; GTRD, gene transcription regulatory database; GTT, glucose tolerance test; H&E, hematoxylin and eosin; Hbonds, hydrogen bonds; HFD, high-fat diet; HFHC, high-fat and high-cholesterol; HOMA-IR, homeostatic model assessment of insulin resistance; HSCs, hepatic stellate cells; IP, immunoprecipitation; ITT, insulin tolerance test; K, dissociation constant; KEGG, kyoto encyclopedia of genes and genomes; KPBS, potassium phosphate-buffered saline; LC-MS/MS, liquid chromatography-tandem mass spectrometry; LW/BW, liver-to-body weight ratio; MAP1LC3/LC3, microtubule associated protein 1 light chain 3; MASH, metabolic dysfunction-associated steatohepatitis; MASLD, metabolic dysfunction-associated steatotic liver disease; MCD, methionine and choline deficient; MST, microscale thermophoresis assay; MTOR, mechanistic target of rapamycin kinase; MTORC1, MTOR complex 1; ND, normal diet; NFKB/NF-κB, nuclear factor kappa B; NFKBIA/IKBA, NFKB inhibitor alpha; OP, oleate acid and palmitate acid; PBS, phosphate-buffered saline; PCA, principal component analysis; qRT-PCR, real-time quantitative PCR; RELA/p65, RELA proto-oncogene, NF-kB subunit; Res, resmetirom; Rg, radius of gyration; RMSD, root-mean-square deviation; RMSF, root-mean-square fluctuation; RPS3, ribosomal protein S3; RPS6KB1/S6K1, ribosomal protein S6 kinase B1; RRAGC, ras related GTP binding C; SASA, solvent-accessible surface area; SNRPD2, small nuclear ribonucleoprotein D2 polypeptide; SQSTM1/p62, sequestosome 1; T, half-life; TFE3, transcription factor binding to IGHM enhancer 3; TFEB, transcription factor EB; TMEM192, transmembrane protein 192; VIM, vimentin; WT, wild-type. - Source: PubMed
Publication date: 2026/05/25
Du XiliangFang ZhiyuanLiu GuowenWang LiJu LingxueGao WenwenSong YuxiangLei LinLi Xinwei - Rare coding genetic variants may exert large effects on risk of common disease, yet their contribution to disease architecture and their utility in gene prioritization remain limited by inadequate sample sizes. Here, we performed a massive-scale rare variant association study (RVAS), analyzing over 1.1 million sequenced participants among which 130,000 had atrial fibrillation (AF). Through a multi-mask burden testing approach, we identified 15 genes significantly associated with AF through rare large-effect variation. Integrative analyses revealed strong convergence between genes implicated by rare and common variation, and highlighted instances where RVAS data may aid in GWAS prioritization. Nevertheless, several RVAS genes were not among GWAS loci ( , , , ), or were not nominated through contemporary GWAS prioritization ( , ). Finally, we observed that ultra-rare protein-disrupting variants - concentrated in a small number of large-effect size genes - explained at least 2% of AF susceptibility across European and African ancestry groups. These findings refine the genetic architecture of AF, while highlighting the value and cost of RVAS for genomic discovery in common disease. - Source: PubMed
Publication date: 2026/05/04
Jurgens SeanEnzan NobuyukiDinsmore IanChoi Seung HoanLuo JonathanLipov AlexHartle CassandraWang XinMarston NicholasWeng Lu-ChenMelloni GiorgioChalazan BrandonGray MichaelPirruccello JamesDiaz AnnetteChaffin MarkOrnelas-Loredo AylinTang OwenDarbar FaisalKany ShinwanChen Yiningvon Falkenhausen AenneMorrison AlannaNatale AndreaTveit ArnljotGeelhoed BastiaanCade BrianWagoner David VanHaase DoreenSoliman Elsayed ZDavogustto GiovanniCalkins HughAnderson JefferyBrody JenniferBarnard JohnHokanson JohnSmith JonathanBis JoshuaYoung KendraJohnson LindaLong LeannRisch LorenzGula LorneKwee LydiaKühne MichaelPreuss MichaelGupta NamrataNafissi NavidSmith NicholasNilsson Petervan der Harst PimWells QuinnJudy RenaeSchnabel RenateJohnson ReneeSmit Roelof A JGabriel StaceyKnight StaceyFurukawa TetsushiMin Yuan-IYoneda ZacharyLaksman ZacharyAlonso AlvaroPsaty BruceAlbert ChristineArking DanRoden DanChasman DanielRader DanielConen DavidMcManus DavidFatkin DianeBoerwinkle EricMarcus GregoryChristophersen IngridSmith J GustavRoberts JasonRaffield LauraShoemaker M BenjaminCho MichaelCutler MichaelChung MinaOlesen MortenSinner MoritzSotoodehnia NonaKirchhof PaulusLoos Ruth J FNazarian SamanMohanty SanghamitraDamrauer ScottKaab StefanHeckbert SusanRedline SusanShah SvatiTanaka ToshihiroEbana YusukeLubitz StevenLunetta KathrynBenjamin EmeliaRienstra MichielFigtree GemmaDarbar DawoodBezzina ConnieRuff ChristianSabatine MarcMirshahi ToorajEllinor Patrick - Hepatopancreatic microsporidiosis (HPM) in Litopenaeus vannamei caused by Ecytonucleospora hepatopenaei (EHP) mainly manifests as growth retardation. Hitherto, the mechanism by which it inhibits growth remains unclear. In this study, muscle transcriptome sequencing was conducted on shrimp artificially challenged with EHP for 10 d, and the expression characteristics of genes related to the mTOR pathway were investigated to explore the molecular mechanism underlying muscle growth inhibition in EHP-infected shrimp. A total of 1289 differentially expressed genes were identified, including 726 up-regulated and 563 down-regulated genes. Significant down-regulation of growth-related genes was detected in EHP-infected shrimp, especially those encoding actin and myosin. Moreover, the expression levels of cell division-related gene cyclin dependent kinase 1 (CDK1) and the molting-related gene β-N-acetylhexosaminidase 20 (HEX) were also significantly inhibited. However, the gene expression of mTOR and its related negative regulatory factors (unc-51, Tsc1 and FNIP1) was significantly up-regulated, along with immune-related genes such as anti-lipopolysaccharide factor (ALF) and prophenoloxidase-activating factor 3 (PPAF3). In contrast, the expression of NLR family CARD domain containing 4 (NLRC4) was significantly down-regulated. Functional enrichment analyses revealed that EHP infection mainly affected protein synthesis and glucose metabolism pathways. Furthermore, the expression of key genes in the mTOR pathway was detected to be significantly up-regulated within 20 d post EHP challenge. These findings indicate that EHP infection triggered an immune response and disrupted muscle cell division, protein synthesis, and molting processes, providing valuable resources for clarifying the molecular mechanism of growth regulation in shrimp after EHP infection. - Source: PubMed
Publication date: 2026/05/08
He ChuanyuYin ZhipengTian YajieYang FanCao ZhengWang CuixiaYan DongchunLi TingChang LinruiSi Lingjun - As the mechanism of myocardial injury caused by fluoride is still unclear, the study is to investigate whether the effects of fluorosis on heart involve changes in lysosomal biogenesis and autophagic flux. - Source: PubMed
Publication date: 2026/05/06
Liao WeiTu XiDeng JieXiang JieHe Wen-WenXiao XiaoZeng Xiao-XiaoDong Yang-TingQi Xiao-LanXiao YanHong WeiHe YanLou Di-DongGuan Zhi-Zhong - Acute myeloid leukemia (AML) is a highly lethal hematologic malignancy, and reliable prognostic biomarkers remain urgently needed. We investigated the expression and clinical relevance of the actin cytoskeleton regulator N-WASP in AML. Analysis of TCGA data revealed significantly reduced N-WASP expression in AML compared with normal tissues, and low expression was associated with adverse clinical features, including FAB-M1/M4 subtypes, DNMT3A mutations, and cytogenetic abnormalities such as t(8;21)/RUNX1::RUNX1T1 and del(7q). Patients with low N-WASP expression exhibited shorter overall survival, and multivariate Cox regression identified N-WASP reduction as an independent risk factor, alongside advanced age and FLT3, DNMT3A and TP53 mutations. Co-expression and enrichment analysis highlighted FNIP1, CLIP1, RICTOR and BRAF as N-WASP-associated regulators converging on mTOR signaling. Experimental validation via RT-qPCR and western blotting in AML bone marrow samples and cell lines confirmed the downregulation of N-WASP and key co-expressed genes. Collectively, these results demonstrate that N-WASP is suppressed in AML and is closely associated with disease risk and clinical outcome. N-WASP may serve as a novel prognostic biomarker and potential therapeutic target warranting further investigation. - Source: PubMed
Publication date: 2026/04/22
Liu CuiSun JianLuo YanHuang PeiChen Yan