HTLV p19 antigen ELISA
- Known as:
- HTLV p19 antigenic Enzyme-linked immunosorbent assay test
- Catalog number:
- GEN0801116
- Category:
- Peptides
- Supplier:
- Bio-gentaur
- Gene target:
- HTLV p19 antigen ELISA
Related genes to: HTLV p19 antigen 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 p19 antigen ELISA
Related articles to: HTLV p19 antigen ELISA
- CNS vascular endothelial cells (ECs) exhibit a distinctive gene expression program that is foundational for the blood-brain barrier (BBB). Previous research identified candidate cis-regulatory elements (CREs) that were hypothesized to control this program. In this work, transgenic mice and recombinant adeno-associated virus (rAAV) vectors have been used to interrogate these candidate CREs in vivo. These experiments show that an 850 bp genomic DNA segment ∼60 kb 5' of Slc2a1 possesses enhancer activity that is (1) specific for BBB+ CNS ECs and (2) both necessary and sufficient for BBB+ EC gene expression. A screen of >8,000 genomic DNA segments from CNS EC-specific CRE candidates reveals several hundred with enhancer activity. Transcription factors ERG and LEF1 are shown to occupy sites in brain ECs that are highly enriched in candidate and experimentally validated CREs, lending strong support to a model in which canonical Wnt signaling activates the BBB program via LEF1. - Source: PubMed
Publication date: 2026/03/30
Li ZhongmingRattner AmirWang YanshuSmallwood Philip MSabbagh MarkMannion Brandon JPennacchio Len ANathans Jeremy - To investigate the potential toxicological effects of acetyl tributyl citrate (ATBC) on osteoarthritis (OA) and elucidate the underlying mechanisms using bioinformatics, machine learning, and network toxicology. - Source: PubMed
Publication date: 2026/02/02
Zhu YifangDeng LinXia JunxiangYang JingZhao DanLi Min - : This study aimed to investigate the phytochemical composition, antioxidant capacity, and anticancer potential of methanol and ethanol extracts of (L.) Gray in MCF-7 breast cancer cells, focusing on their effects on energy metabolism and related molecular mechanisms. In samples, total antioxidant activity and total phenolic content were determined spectrophotometrically, while individual phenolics were classified by HPLC and volatile aromatic compounds (VOCs) were determined by GC-MS. The anticancer effects of in MCF-7 breast cancer were determined using RT-qPCR with 46 different genes. Phytochemical profiling via HPLC and GC-MS revealed a rich diversity of bioactive compounds, including significant levels of gallic acid (298.89 µg/g), vanillic acid (191.98 µg/g), and succinic acid (724.73 µg/g). The extracts exhibited robust antioxidant activity and dose-dependent cytotoxicity, reducing cell viability to as low as 5.60% after 72 h. Molecular analysis through Reactome pathway enrichment and expression profiling of 46 genes demonstrated that drives cancer cells into a metabolic impasse by reversing the Warburg effect. Key findings include the significant downregulation of glycolytic genes like / (-12.34) and (-1.71), alongside the repression of mitochondrial TCA cycle regulators such as (-17.81) and (-2.54). This metabolic collapse triggered G0/G1 phase cell cycle arrest and induced apoptosis. : These results align with international benchmarks for species while providing novel insights into the metabolic reprogramming mechanism. The results obtained in this study highlight that emerges as a promising natural agent for therapeutic strategies targeting cancer bioenergetics. - Source: PubMed
Publication date: 2026/03/23
Gülüm LeventGüler EmrahÇapkınoğlu EmirÇelik Ayşe BüşranurTutar Yusuf - Erythroid acute myeloid leukemia (AML) cell line OCI-M2 expresses a particular oncogenic network: IRF6, in concert with ETV2 and HEY1, aberrantly activates NKL homeobox gene NKX2-4, which in turn represses megakaryocytic lineage factor FLI1. Interestingly, in keratinocytes, IRF6 is able to bind glucose which promotes IRF6-dimerization and thus alters its binding site selection. Here, we used OCI-M2 as a model to investigate the role of glucose level and IRF6 in leukemogenesis. Treatment of OCI-M2 with high glucose or 2-deoxy-glucose resulted in the downregulation of IRF6 and NKX2-4, and the upregulation of FLI1, indicating that glucose-mediated dimerization of IRF6 altered its reported autoactivation. The screening of this cell line for genes encoding glycolytic enzymes identified aberrant overexpression of glucose-6-phosphate isomerase (GPI) and phosphofructokinase L (PFKL), which were targeted by genomic amplification and chromothripsis-like alterations, respectively. Furthermore, GPI was activated by NKX2-4 and ETV2, and PFKL by ETV2. Finally, siRNA-mediated downregulation of PFKL resulted in elevated glucose levels, suppressed expression of IRF6 and NKX2-4, and activated FLI1. Thus, we connected an oncogenic regulatory network with deregulated glycolytic enzymes and glucose metabolism, thereby establishing a new in vitro model to develop novel therapeutic avenues in AML subsets. - Source: PubMed
Publication date: 2026/03/23
Nagel StefanMeyer CorinnaPommerenke Claudia - Syndrome-specific International Classification of Diseases, 10th Revision (ICD-10) codes have the potential to improve identification of patients for precision therapies, clinical trials, and research, yet their real-world uptake is not well characterized. We evaluated the utilization of syndrome-specific ICD-10 codes at a large academic medical center among patients with pathogenic or likely pathogenic variants in 10 monogenic epilepsy genes with established codes (CDKL5, EHMT1, KCNQ2, MECP2, MED13L, SCN1A, SHANK3, SLC13A5, SLC2A1, SYNGAP1). Patients were identified from an institutional genetic testing database and were included if they had at least one clinical encounter after code implementation or genetic diagnosis. Variants of uncertain significance were manually curated, and Rett and Dravet phenotypes were reviewed for accuracy. Of 83 patients with qualifying variants, 39 met inclusion criteria. Only 56.4% (22/39) were ever assigned a syndrome-specific ICD-10 code, which appeared in 31.1% of encounters and accounted for 14.5% of all documented codes. Uptake varied by syndrome, provider specialty, and encounter type and increased over time. In the Dravet syndrome subgroup (n = 23), generic epilepsy codes were documented more than twice as often as the Dravet-specific code (G40.83). When G40.83 was documented, other epilepsy codes were used less frequently, suggesting it may be treated as a substitute for broader epilepsy codes. These findings demonstrate inconsistent and limited adoption of syndrome-specific ICD-10 codes, highlighting the need for improved coding support and integration of structured genetic data within the electronic health record. - Source: PubMed
Publication date: 2026/03/26
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