Quadruple sampling port with fittings
- Known as:
- Quadruple sampling port fittings
- Catalog number:
- 800051
- Category:
- -
- Supplier:
- Lambda Laboratory Instruments
- Gene target:
- Quadruple sampling port with fittings
Related genes to: Quadruple sampling port with fittings
- Gene:
- SNUPN NIH gene
- Name:
- snurportin 1
- Previous symbol:
- RNUT1
- Synonyms:
- SNURPORTIN-1, Snurportin1
- Chromosome:
- 15q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-10
- Date modifiied:
- 2014-11-19
Related products to: Quadruple sampling port with fittings
12 Port Gassing Manifold For Innova 4212 Port Gassing Manifold For Innova 4312 Port Gassing Manifold For Innova 448-Port Manifolds8-Port Manifolds Sterile, Indiv. Wrapped8-Port Manifolds Sterile, Indiv. Wrapped8-Port Manifolds Sterile, Indiv. WrappedA sampling of each type of bead in a 10 mL tubeAdditional pump line e.g. for feed (MULTIFLOW, reagent bottle with pipes, fittings, filter, tubing)Additional pump line e.g. for harvest (PRECIFLOW, reagent bottle with pipes, fittings, filter, tubing)As above but fitted with pressure relief value, inlet port and gromet for electrical cableAs above but fitted with pressure relief value, inlet port and gromet for electrical cableAs above but fitted with pressure relief value, inlet port and gromet for electrical cableAs above but fitted with pressure relief value, inlet port and gromet for electrical cableAs above but fitted with pressure relief value, inlet port and gromet for electrical cable Related articles to: Quadruple sampling port with fittings
- OBJECTIVE To identify circulating proteins associated with type 2 diabetes (T2D) risk through pathways not fully explained by body mass index (BMI), and to assess therapeutic actionability. RESEARCH DESIGN AND METHODS We applied GWAS-by-subtraction within a genomic structural equation model to European ancestry summary statistics for T2D (74,124 cases, 824,006 controls) and BMI (n = 681,275), partitioning T2D liability into BMI-related and BMI-subtracted components. We then performed proteome-wide Mendelian randomization (MR) using cis-protein quantitative trait loci from four plasma proteomics cohorts: ARIC, deCODE, Fenland, and the UK Biobank Pharma Proteomics Project. Prioritized proteins passed sensitivity analyses with alternative MR methods and were supported by colocalization evidence. Tissue-resolution regulatory support was assessed using cis-eQTL colocalization across GTEx and pancreatic islet, subcutaneous adipose, and whole-blood resources. Actionability was evaluated using the druggable genome and Open Targets. RESULTS GWAS-by-subtraction attenuated the genetic correlation between BMI and BMI-subtracted T2D from 0.54 (SE 0.02) to 0.35 (SE 0.02). Proteome-wide MR prioritized 29 proteins for BMI-subtracted T2D. Thirteen showed eQTL colocalization in at least one tissue, implicating liver and intermediary metabolism (GCDH, NOTCH2), pancreatic islet biology (CTRB2, MANBA), adipose and Wnt signaling (RSPO3, GALNT3), and whole blood regulatory signals (PAM, SNUPN). Sixteen proteins were classified within druggable-genome Tiers 1-3, and five had existing Open Targets compounds. CONCLUSIONS Integrating GWAS-by-subtraction, proteome-wide MR, and colocalization nominated 29 proteins associated with T2D liability not fully explained by BMI. These findings highlight genetically supported targets for follow-up studies of T2D therapies that complement weight-centered approaches. - Source: PubMed
Publication date: 2026/06/22
Su Chen-YangLu Tianyuan - Myocardial infarction (MI) is a myocardial necrosis event caused by an unstable ischemic state that reduces life expectancy primarily through cardiac functional impairment and cardiomyocyte death. The present study aims to investigate the genetic mechanisms underlying MI by integrating expression quantitative trait loci (eQTLs) and Mendelian randomization (MR) analyses. - Source: PubMed
Publication date: 2026/03/11
He PeichunLv XiangwenFu ChuwenQin ZhenChen SiyuanZhao JinminXie Jian - Intracranial aneurysm (IA) rupture causes severe brain hemorrhage with high mortality, yet its molecular drivers remain unclear and better risk prediction is urgently needed. Using transcriptomics, single-cell analysis, and genetic data, we investigated the role of N7-methylguanosine (m7G) RNA modification in IA. We identified distinct m7G modification patterns, validated their methylation features in patient samples, and incorporated these patterns into a machine learning-based rupture prediction model. The presence and characteristics of m7G patterns significantly improved model performance, achieving high predictive accuracy across three independent cohorts (AUC 0.91-0.95). Genetic analyses further identified three causal m7G-related genes (NSUN2, IFIT5, SNUPN), and laboratory experiments confirmed their altered expression and methylation in ruptured aneurysms. Overall, our findings demonstrate that m7G modifications play a key role in IA rupture. The validated prediction model offers strong clinical potential for rupture risk assessment, and the identified genes represent promising therapeutic targets. - Source: PubMed
Publication date: 2026/03/12
Wu PengfeiMaimaiti AierpatiMa ZekunAbulizi AlimasiYang WenboYin ShengnanWang YongxinWang Zengliang - Mutations in the SNUPN gene, which encodes snurportin-1, a nuclear import adaptor for U1 small nuclear ribonucleoproteins (snRNP), have recently been implicated in limb-girdle muscular dystrophy, attributed to disrupted pre-messenger RNA splicing in skeletal muscle. U1 small nuclear ribonucleoproteins play a vital role in pre-messenger RNA splicing, a process essential for transcript fidelity and the regulation of gene expression across tissues. However, the impact of SNUPN mutations on the CNS remains unclear. We identified pathogenic variants in the SNUPN gene in two families with spinocerebellar atrophy. One patient exhibited mild changes in skeletal muscle, while the other did not. To elucidate the pathogenic mechanisms, nuclear transport of the mutated snurpotin-1, and its interaction with importin beta were analysed in vitro. Then, we generated a knock-in mouse carrying the patients' variants and assessed its motor function and cerebellar morphology in vivo. Furthermore, we analysed U1 snRNP localization and RNA splicing in cerebellar Purkinje cells by both RNA- and single-cell RNA sequencing. Mutated snurportin-1 displayed impaired nuclear transport and reduced binding to importin beta. The knock-in mouse mimicking the compound heterozygous variants exhibited cerebellar ataxia, cerebellar atrophy and dendritic abnormalities in Purkinje cells. Abnormal RNA splicing and reduced expression were observed in many genes related to neuronal development and synaptic organization in Purkinje cells, leading to an immature cytoskeleton and reduced secretion of sonic hedgehog. The defects in Purkinje cells caused secondary abnormalities in granule cell migration and interneuron development. Our findings suggest that snurportin-1 plays a critical role in cerebellar development through U1 snRNP-mediated RNA processing and that its dysfunction may contribute to spinocerebellar ataxia. These results expand the clinical spectrum of SNUPN-related disorders beyond skeletal muscle and highlight splicing dysregulation as a potential mechanism underlying cerebellar atrophy. - Source: PubMed
Okubo MarikoOgawa MegumuEura NobuyukiInoue Yukiko UDewa Ken-IchiOwa TomooMiyashita SatoshiMurakami TerumiNakamura HisayoshiHayashi ShinichiroNonaka IkuyaOgata KatsuhisaHoshino MikioInoue TakayoshiNishino IchizoNoguchi Satoru - Bioavailable testosterone (BAT), a critical factor for reproductive, metabolic, and psychological health, is primarily regulated by sex hormone-binding globulin (SHBG). However, the molecular mechanisms driving SHBG-mediated regulation of BAT remain unclear. Identifying key protein regulators offers promising therapeutic opportunities for testosterone-related disorders. We conducted a comprehensive proteome-wide Mendelian randomization (PWMR) and colocalization analysis using large-scale pQTL and GWAS datasets. Mediation MR assessed SHBG's role in regulating BAT, and functional enrichment, protein interaction networks, phenome-wide association studies (PheWAS), and drug prediction were performed to explore therapeutic relevance and safety. We identified 36 proteins that influence BAT via SHBG mediation. Among them, five proteins (MAX, TXNL4B, GLRX2, F13B, SNUPN) showed strong or moderate colocalization with BAT, suggesting shared genetic regulation. MAX and TXNL4B increased BAT by reducing SHBG, while GLRX2, F13B, and SNUPN decreased BAT via elevated SHBG levels. PheWAS suggested potential risks for GLRX2 (depression) and TXNL4B (lipid disorders). Drug and compound prediction highlighted compounds, including cardiac glycosides, antioxidants, and endocrine-disrupting chemicals, targeting these proteins. Our findings reveal novel protein regulators of testosterone bioavailability through SHBG and provide a framework for developing targeted therapeutics. This integrative approach may support safer, more precise treatment strategies for testosterone-related metabolic and endocrine disorders. - Source: PubMed
Publication date: 2025/10/24
Hong Yanggang