HTLV 1+2 ELISA
- Known as:
- HTLV 1+2 Enzyme-linked immunosorbent assay test
- Catalog number:
- Ⅰe012
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Glory bioscience
- Gene target:
- HTLV 1+2 ELISA
Related genes to: HTLV 1+2 ELISA
- 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 1+2 ELISA
Related articles to: HTLV 1+2 ELISA
- Brain microvascular endothelial cells (BMECs) form the blood-brain barrier (BBB), a highly selective interface that restricts paracellular diffusion and regulates the transport of nutrients and drugs into the central nervous system via specialized transporters and receptors. Tight junction-associated protein 1 (Tjap1), also termed protein incorporated later into tight junctions (Pilt), has been localized to tight junctions (TJs) in epithelial cells and to the trans-Golgi network in fibroblasts; however, its expression, subcellular localization, and functional significance in BMECs are still unknown. We characterized Tjap1 subcellular localization in mouse and human BMEC cell lines as well as primary mouse BMECs by immunofluorescence with and without pharmacological Golgi disruption by treatment with Brefeldin A, Golgicide A or Pitstop 2. CRISPR/Cas9-mediated Tjap1 knockout cells were generated and examined with regard to their Golgi morphology using immunostaining. Tjap1 mRNA localization was examined by RNAscope in situ hybridization. Quantitative real-time PCR and Western blot was performed to assess the expression of BBB-associated efflux transporters, solute carrier transporters, and cellular receptors in control and Tjap1 knockout cells. Tjap1 predominantly localized to the cis-Golgi compartment, co-localizing with Gm130 rather than Tgn38, and was absent from TJs in BMECs. Tjap1 knockout induced pronounced Golgi fragmentation BMECs. Importantly, Tjap1 knockout significantly downregulated mRNA-expression of Abcb1a, Abcb1b, Abcc4, Slc2a1, Slc7a1, Slc7a5 and Tfrc, while Abcg2 was upregulated. At the protein level, a decrease in the protein levels of Abcb1, Abcc4, Slc2a1, Slc7a1, and Tfrc was observed in Tjap1 knockout cEND cells. In BMECs, Tjap1 is a cis-Golgi-associated protein required for the structural integrity of the Golgi apparatus. Its deletion is associated with Golgi fragmentation and significant alterations in the mRNA and protein expression of drug transporters and receptors at the BBB. These findings identify Tjap1 as a candidate regulator of both Golgi architecture and the BBB transporter profile in vitro, with potential implications for modulating drug transport across the BBB. - Source: PubMed
Publication date: 2026/05/28
Mi JunqiaoSchoder AnnabelleSun AiliMeybohm PatrickBurek Malgorzata - Epidemiological and biological evidence indicate a close connection between Alzheimer's disease (AD) and type-2 diabetes mellitus. Glucose transporter 1 (GLUT1), encoded by the gene, has a major role in glucose metabolism, the dysregulation of which has been implicated in both diseases. We conducted a case-control association study in a sample of 439 non-diabetic patients with late-onset AD and 304 cognitively healthy, non-diabetic elderly controls to determine the potential risk for developing AD associated with rs841847 polymorphism. The rs841847 C/C genotype occurrence was higher in the AD group (AD: 60.4%, controls: 50.7%), while the minor T allele-containing genotypes were more frequent among controls (AD: 39.6%, controls: 49.3%). A multivariate logistic regression model adjusted for age, sex, and apolipoprotein E () ε4 status (ε4 allele carriers versus non-carriers) demonstrated that carriers of the T allele had a significantly reduced risk for AD compared to C/C homozygotes (OR = 0.672; 95% CI: 0.493-0.916; = 0.012). Although the rs841847 polymorphism has been linked to type-2 diabetes mellitus, the present study investigated this gene variant in AD for the first time. Our findings indicate a moderate protective effect for the rs841847 T allele on the susceptibility to AD. We demonstrated the rs841847 polymorphism as a candidate single nucleotide polymorphism for further examination as a predisposing genetic factor for AD. - Source: PubMed
Publication date: 2026/05/29
Fehér ÁgnesBoldizsár AnnaPákáski MagdolnaJanka ZoltánKálmán János - Proliferative diabetic retinopathy (PDR) is one of the leading causes of blindness in working-age adults. We have previously shown that the risk of PDR is significantly elevated in individuals with intrauterine exposure to famine. However, the genetic mechanisms mediating this association remain unknown. The aim of the current study was to investigate the molecular underpinnings of famine-related PDR by performing genome-wide association (GWAS) and interaction studies (GWIS). - Source: PubMed
Publication date: 2026/06/25
Fedotkina OlenaBegum Most ChampaTrinh Xuan TungÖzgumus TurkulerÅkerlund MikaelNilsson PeterSpindola Leticia MariaLyssenko Valeriya - To clarify how steaming and sun-drying cycles affect the hepatic risk-benefit profile of Polygoni Multiflori Radix (PMR), the herb was processed with black bean decoction for 1-9 cycles following the traditional "nine steaming and nine sun-drying" protocol. UPLC-MS analysis showed that anthraquinones and trans-THSG progressively decreased with increasing cycles and stabilized after five cycles, whereas cassialactone-8-O-β-D-glucoside and hyperoside emerged as new components during processing. In a low-dose LPS-sensitized mouse model mimicking immune-idiosyncratic liver injury, PMR processed for three or more cycles significantly alleviated liver damage. In an acetaminophen (APAP)-induced acute liver injury model, PMR processed for 5-7 cycles exhibited the strongest hepatoprotective effects. Spectrum-effect correlation analysis identified twelve constituents (e.g., emodin-8-O-β-D-glucoside) associated with liver injury, involving targets related to drug metabolism (CYP3A4), membrane transporters (ABCB1, SLC2A1), and oxidative stress (SOD1). Five components (e.g., cassialactone-8-O-β-D-glucoside) were linked to hepatoprotection, potentially through modulation of synthetic function (ALB) and inflammatory response (TNF, EGFR, HSP90AA1). The Cellular Thermal Shift Assay (CETSA) was employed to validate the molecular docking results, demonstrating that emodin-8-O-β-D-glucopyranoside and physcion-8-O-β-D-glucoside significantly enhanced the thermal stability of TP53. In parallel, emodin and hyperoside were confirmed to increase the thermal stability of albumin (ALB). Overall, processing PMR with black bean decoction for 5-7 cycles is optimal for reducing hepatic risk while preserving or enhancing hepatoprotective activity. These findings support a risk-benefit-oriented processing standard and propose candidate quality markers for standardized manufacturing, including trans-THSG, emodin, aloe-emodin, cassialactone-8-O-β-D-glucoside, and hyperoside. - Source: PubMed
Publication date: 2026/06/23
Zhang HuijieZhao XiaoranWang FangyuLiu MengQin XiupingSun HaoLiang YingRen XiaoliangLiu YananPu Weiling - Neoadjuvant chemoradiotherapy (CRT) constitutes a standard treatment for locally advanced rectal cancer (RC), frequently followed by radical surgical resection. Yet, therapeutic responses vary widely, and intrinsic radioresistance remains a major barrier to cure. To uncover actionable determinants of CRT response, we established a panel of patient-derived colorectal cancer cell lines (PDCLs) followed by integrated phenotypic and functional characterization. We identified metabolic reprogramming as a hallmark of radioresistance and, through orthogonal validation experiments, confirmed elevated glycolytic and mitochondrial ATP production in (chemo)irradiation-resistant PDCLs. The causative relationship of this association and its potential for therapeutic intervention was shown by subsequent drug screening, showing resistance to most of the applied drugs and revealing a critical dependency on the monocarboxylate transporter (MCT1) and the glucose transporter 1 (GLUT1). Metabolism-targeting compounds re-sensitized resistant PDCLs to irradiation; especially inhibition of GLUT1 exhibits a robust radiosensitizing activity across models. Concordantly, GLUT1 expression correlated with poor response to neoadjuvant CRT in our own RC patient cohort and various publicly available patient datasets. Collectively, our study defines metabolic dependency as a key driver of CRT resistance in RC, and reveals glycolysis- and lactate-transport-associated pathway activities as targetable vulnerabilities. These findings provide a mechanistic basis for patient stratification and support the development of metabolism-directed strategies to overcome (chemo)radioresistance in RC. - Source: PubMed
Publication date: 2026/06/23
Hellkamp MaximilianGertken SimonBuchloh JonasHellwig Julius-LeonardKowitzke Lukas BenDuan NingjunGaspardo IlariaKüffer StefanLinnebacher MichaelStröbel PhilippWirth MatthiasEllenrieder VolkerRieken StefanGaedcke JochenGhadimi MichaelWienands JürgenSchneider GünterSpitzner MelanieGrade Marian