HTLV I&II Ab screening ULTRA
- Known as:
- HTLV I&II Antibody detection ULTRA
- Catalog number:
- HTLVABULTRA.CE
- Product Quantity:
- 192 Tests n
- Category:
- -
- Supplier:
- DiaPro
- Gene target:
- HTLV & screening ULTRA
Related genes to: HTLV I&II Ab screening ULTRA
- Gene:
- SLC2A1 NIH gene
- Name:
- solute carrier family 2 member 1
- Previous symbol:
- GLUT1, GLUT, HTLVR, CSE
- Synonyms:
- DYT18, DYT9
- Chromosome:
- 1p34.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-11-18
- Date modifiied:
- 2019-04-23
Related products to: HTLV I&II Ab screening ULTRA
*Letheen Agar,Modified USE For screening cosmetic products for microbial contamination.*Letheen Broth,Modified USE For screening cosmetic products for microbial contamination as per FDA.*Modified Letheen Agar USE For screening cosmetic products for microbial contamination.*Modified Letheen Broth USE For screening cosmetic products for microbial contamination as per FDA.0.1ml 4-Strip Tubes & Strip Ca Corbett-type, Ultra Thin Wall0.1ml 4-Strip Tubes & Strip Ca Corbett-type, Ultra Thin Wall0.1ml 4-Strip Tubes & Strip Ca Rotorgene-type,Ultra Thin Wall0.1ml 8-Strip PCR Tubes & Caps Ultra Thin Wall, Low Profile0.1ml 8-Strip PCR Tubes & Caps Ultra Thin Wall, Low Profile0.1ml 8-Strip PCR Tubes & Caps Ultra Thin Wall, Low Profile0.1ul-10ul Ultra Micro Tip0.2ml 8-well Max Recovery Ultra Thin Wall PCR Tubes0.2ml 8-well Max Recovery Ultra Thin Wall PCR Tubes0.2ml PCR Tube, Flat Cap Ultra Thin Wall per Max Recovery0.2ml PCR Tube, Flat Cap Ultra Thin Wall/Max Recovery Related articles to: HTLV I&II Ab screening ULTRA
- Cyclotriphosphazenes (CTPs), widely used as lithium-ion battery electrolyte additives, are increasingly recognized as environmental contaminants with potential neurotoxicity. We developed an integrated computational framework to evaluate the blood-brain barrier (BBB) penetration potential and neurotoxic mechanisms of CTPs. Six representative CTPs were predicted to penetrate the BBB via passive diffusion and impair BBB function. Among them, HPCTP, PFPCTP, HCCTP, and HFCTP primarily disrupted BBB function through inhibition of ATP-binding cassette transporters. HPCTP exhibited the strongest BBB-disrupting potential, primarily through interactions with SLC2A1 and SLC6A3 and through the modulation of BBB-related gene expression. Experimental validation in hCMEC/D3 cells showed that HPCTP impaired glucose transport and utilization and significantly downregulated SLC2A1 expression. These findings provide a strategy for assessing BBB penetration of exogenous chemicals and highlight the potential CNS risks associated with environmental CTP exposure. - Source: PubMed
Publication date: 2026/08/13
Yang QiyuZhang JinmingDao YuxuanHe ZhengruiLu RuiJaman RummanaWu YaoleLiu ShuqiZhang ConglinZhang ZhibiZhou Jiaqi - Extracellular vesicles (EVs) are increasingly recognized as active coordinators of metabolic processes rather than mere messengers. By carrying unique subsets of enzymes, metabolites, lipids, and nucleic acids, EVs can directly deliver functional metabolic machinery or dynamically alter intracellular metabolic fluxes in recipient cells. However, their role in regulating specific biochemical pathways remains largely unknown. - Source: PubMed
Publication date: 2026/08/07
Kashyap Namita NBhat Sharath MohanUdupa E G PadmanabhaShettigar Kavitha SBhat Vinutha RUpadhya Dinesh - Metformin has anticancer potential, but benefit in colorectal cancer (CRC) is heterogeneous and determinants of tumor cell response remain unclear. We tested whether extracellular glucose and the relative expression of glucose transporter 1 (GLUT1/SLC2A1) and sodium-glucose cotransporter 1 (SGLT1/SLC5A1), quantified as a glucose transporter ratio score (GTRS), are associated with buffering of metformin effects. We combined a 1,2-dimethylhydrazine (DMH)-induced CRC model, glucose-controlled cell-line experiments, and analyses of public bulk, single-cell, and spatial transcriptomic datasets. In mice, metformin (200 mg/kg/day) reduced DMH-associated neoplastic progression and Cyclin D1 expression. In vitro, metformin (5 mM) reduced viability and clonogenic growth while reducing endolysosomal acidity and inhibiting mTORC1 downstream signaling under normal glucose. Metformin-induced changes were attenuated under high glucose. Buffering of lysosomal acidity loss was stronger in the GTRS-high HCT116 cells than in the GTRS-low HT29 cells, with partial rescue of growth readouts in both lines. In human single-cell datasets, high-GTRS malignant clusters showed higher lysosome-related transcriptional program scores. In spatial transcriptomic datasets, lysosome-related programs were enriched at the tumor-stroma interface, where stromal laminin ligands and epithelial integrin receptors showed enriched spatial co-localization. In human bulk cohorts, higher GTRS was enriched in the aggressive mesenchymal CMS4 subtype. Together, these results support that glucose transporter balance is associated with partial buffering of metformin-induced lysosomal and mTORC1 perturbations under high glucose. - Source: PubMed
Publication date: 2026/08/21
Allal Badr-EddineMendonça SusanaBounaama AbdelkaderFresco PaulaDjerdjouri BahiaGonçalves JorgeVelho Sergia - Fetal health is heavily dictated by the maternal environment. Inhaling airborne pollutants, like particulate matter, is associated with pregnancy complications and fetal developmental pathologies, including fetal growth restriction (FGR). Because fetal growth is dependent on the placental transfer of nutrients from the maternal circulation, particularly glucose, investigating glucose transport capacity is critical to understanding the development of FGR associated with gestational inhalation of particulate matter. Pregnant Sprague Dawley rats were exposed to titanium dioxide nanoparticles (9.8 ± 1.0 mg/m) to model occupational-level exposure to airborne particulates, from gestational day (GD) 5 to GD 19 via whole-body inhalation. Glucose transporters (GLUTs) 1, 3 and 4 were evaluated in term placentas on GD 20 and ex vivo placental perfusion was conducted as a functional assessment of glucose transport. Exposure resulted in a reduction in Glut3 mRNA and GLUT1 protein. However, exposed placentas exhibited a functional adaptation, characterized by increased GLUT4 expression and membrane localization of both GLUT1 and GLUT4. Placental perfusion confirmed these molecular changes, revealing increased glucose flux in exposed placentas compared to control (AUC 95% CI: 77.4 to 127.5 vs 39.1 to 73.6, respectively). Contrary to our hypothesis, exposure to these nanoparticles enhanced glucose transport across the placenta. Here we have demonstrated that inhaling airborne pollutants during pregnancy modulates placental function and nutrient transport mechanisms, which can have direct effects on fetal development. Furthermore, we provide evidence for targeted interventions, aimed at mitigating fetal developmental pathologies. - Source: PubMed
Publication date: 2026/08/13
Seymore Talia NHoffmann SaraLouro PedroGardner CarolGoedken Michael JStapleton Phoebe A - Parabens are antimicrobial preservatives with endocrine-disrupting potential. Because methylparaben (MeP), ethylparaben (EtP), and butylparaben (BuP) differ in alkyl-chain length and biological potency, their comparison may reveal structure-dependent cellular responses. Using K562 chronic myeloid leukemia cells, we compared the effects of MeP, EtP, and BuP on cytotoxicity, metabolic activity assessed by resazurin reduction, proliferation- and stress-related markers, and WNT/β-catenin- and PPARγ-associated signaling. Cells were exposed to MeP, EtP, or BuP for 24 or 48 h; pathway-focused experiments used 1 μM parabens alone or with methyl 3-{[(4-methylphenyl)sulfonyl]amino}benzoate (MSAB), a β-catenin-directed WNT/β-catenin inhibitor, or GW9662, a PPARγ antagonist. MeP did not significantly affect LDH release or resazurin reduction. In contrast, EtP and BuP increased resazurin reduction at nanomolar and low-micromolar concentrations. At 1 μM, this response was not accompanied by marked LDH release, ROS generation, or cell-cycle alterations and therefore did not indicate overt acute cytotoxicity or robust proliferation. This response was accompanied by increased expression of WNT-related and glycolysis-associated genes, including AXIN2, LEF1, SLC2A1, HK2, PDK1, and PFKFB3. Parabens also induced divergent c-MYC regulation, with decreased c-MYC mRNA but increased protein abundance, and modulated PPARγ-associated signaling, antioxidant enzymes, caspase-related responses, and p-p62-related signaling. MSAB and GW9662 modified the resazurin-reduction response; however, these pharmacological effects did not establish direct β-catenin or PPARγ dependence. Overall, EtP and BuP, particularly BuP, produced stronger effects than MeP on resazurin reduction and several WNT/β-catenin-, PPARγ-, and p-p62-associated readouts. - Source: PubMed
Publication date: 2026/08/12
Szychowski Konrad ASkóra Bartosz