FNIP1 Peptide
- Known as:
- FNIP1 Peptide
- Catalog number:
- 46-659p
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- FNIP1 Peptide
Related genes to: FNIP1 Peptide
- 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 Peptide
Related articles to: FNIP1 Peptide
- The 9 Birt-Hogg-Dubé (BHD) International Symposium convened virtually in March 2026. The meeting attracted more than 100 participants internationally and highlighted recent findings in a variety of areas, including genetic insight and molecular understanding of BHD syndrome, also known as the Hornstein-Knickenberg syndrome, structure and function of the tumor suppressor Folliculin (FLCN), therapeutic and clinical advances, as well as patient experiences living with this disease. - Source: PubMed
Publication date: 2026/05/18
Rajan NeilBaba MasayaBallabio AndreaHenske Elizabeth PJacques KatherineMarciniak Stefan JPause ArnimShi WeiSoleimani ManoocherTee Andrew RZoncu RobertoMollapour MehdiLinehan W Marston - 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. - Source: PubMed
Publication date: 2026/05/18
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
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