Anti-Human CD57 FITC 25 tests
- Known as:
- Antibody toHuman CD57 fluorecein 25 tests
- Catalog number:
- 11-0577-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD57 FITC 25 tests
Related genes to: Anti-Human CD57 FITC 25 tests
- Gene:
- B3GAT1 NIH gene
- Name:
- beta-1,3-glucuronyltransferase 1
- Previous symbol:
- CD57, LEU7
- Synonyms:
- GlcAT-P, HNK-1, NK-1
- Chromosome:
- 11q25
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-07
- Date modifiied:
- 2014-11-19
Related products to: Anti-Human CD57 FITC 25 tests
Related articles to: Anti-Human CD57 FITC 25 tests
- Perfluorooctane sulfonate (PFOS), a persistent member of the per- and polyfluoroalkyl substances family, has been increasingly associated with adverse carcinogenic effects; however, the molecular basis by which PFOS may contribute to prostate cancer (PCa) initiation and progression remains poorly defined. In this study, we aimed to systematically elucidate the mechanisms underlying PFOS-associated prostate carcinogenesis, with particular emphasis on the identification of actionable molecular targets and metabolically relevant pathways. By integrating network toxicology, transcriptomic differential analysis, weighted gene co-expression network analysis, multi-algorithm machine learning, single-cell and spatial transcriptomics, metabolomics, and structural modeling, we identified a four-gene core signature consisting of APOF, B3GAT1, CGREF1, and ENTPD5. Among these candidates, ENTPD5 emerged as the most prominent PFOS-associated target, showing marked enrichment in epithelial compartments across both single-cell and spatial datasets. Further integrative analyses converged on purine metabolism as a shared pathogenic vulnerability, and increased ENTPD5 expression was accompanied by elevated adenine abundance, supporting the existence of an ENTPD5-centered metabolic axis. Molecular docking and molecular dynamics simulations further suggested stable binding of PFOS to ENTPD5. In addition, immunohistochemical evidence consistently confirmed ENTPD5 upregulation in prostate cancer tissues. Collectively, our findings support a PFOS-ENTPD5-adenine mechanistic axis that may promote prostate cancer initiation and progression through purine metabolic reprogramming, and provide a potential foundation for the development of exposure-related biomarkers and preventive intervention targets in PCa. - Source: PubMed
Publication date: 2026/06/19
Lei YinLei PanShen GuohangLi XingbinTang HaotongWang RuoyanDai Yupei - Natural killer (NK) cells are effector cells of the innate immune system. The cytokine microenvironment influences NK cell function. Dysregulation of NK cell cytotoxicity can manifest in reproductive disorders and is also observed in tumor-transformed tissues. The search for immunotherapies capable of regulating NK cell activity is therefore relevant. This study aimed to evaluate the effect of the TGFβ signaling pathway inhibitor and the cyclin-dependent kinase (CDK) 7/12/13 inhibitor on the transcriptional profile of NK-92 cell line. In the study, the cytokines TGFβ1, IL-12, IL-15, IL-18, and TNFα, and the TGFβ receptor type 1 (TGFβR1) inhibitor LY3200882 and the CDK7/12/13 inhibitor THZ1 were used. The cells were cultured sequentially in the presence of inhibitors and cytokines, followed by assessment of the gene expression of , , , , , , , , , , and We observed direct effects of the inhibitors on NK cells. LY3200882 increased the expression of and , and reduced . THZ1 increased the expression of , , and , while it reduced and . IL-12, IL-15, IL-18, and TNFα modified the gene expression of some phenotypic and cytotoxic receptors and transcription factors. TGFβ1 increased the expression of , , and . Blocking TGFβ-dependent signaling with LY3200882 abolished TGFβ1 effects. We assessed CD56 presence on NK-92 cell membrane and found its increase in the presence of LY3200882. After LY3200882 treatment, in the presence of TGFβ1 and choriocarcinoma cell line JEG-3, the expression of CD56 receptor on NK cell membrane decreased. Pretreating NK cells with THZ1 decreased the expression of , , and in the presence of TGFβ1. Thus, LY3200882 partially neutralized TGFβ1 effects on the expression of NK cell receptor genes. THZ1 followed by TGFβ1 treatment promoted NK cell transcriptional profile characteristic for CD56dim NK cells. Both LY3200882 and THZ1 affected the NK cell transcription even without cytokine treatment. The independent effects of synthetic inhibitors on NK cells, as well as their influence in the presence of tumor cells, should be considered. - Source: PubMed
Publication date: 2026/04/17
Mikhailova ValentinaMarko OksanaMkrtchyan EdgarSokolov Dmitry - BACKGROUND: Intervertebral disc degeneration (IDD), normally characterized by a loss of nucleus pulposus cells (NPCs), is one of the leading causes of lower back pain and various degenerative spinal disorders and has been regarded as a public health issue because of its heavy social and economic consequences. However, the molecular mechanisms underlying IDD formation and progression are unclear so far, which results in the lack of existing biomarkers or treatments in targeting early degeneration effectively. Novel potential biomarkers for the early diagnosis, prevention and treatment of IDD are urgently needed. METHODS: In this study, miRNA sequencing and qRT-PCR validation were performed on original clinical nucleus pulposus (NP) tissues from our own IDD patient cohort. Furthermore, we applied bioinformatics analysis to the mRNA expression profiles in NP tissues (GSE186542) and whole blood (GSE124272) from IDD patients. We screened key genes and miRNA regulators by conducting overlap analysis. RESULTS: The results showed that 466 differentially expressed miRNAs, 187 downregulated and 279 upregulated significantly, were identified from miRNA sequencing analysis in NP tissues. Overlap analysis with the predicted miRNA targets and the differentially expressed genes (DEGs) in the GSE186542 database exhibited 27 overlapping genes, among which copine-6 (CPNE6) and beta-1,3-glucuronyltransferase (B3GAT1) overlapped with the DEGs from the whole blood of IDD patients in the GSE124272 database. Further qRT‒PCR results revealed that CPNE6 and B3GAT1 expression was significantly upregulated, but their corresponding miRNA regulators miR-3620-5p and miR-6511b-3p were significantly downregulated in IDD patients. Moreover, cells proliferation was inhibited, but the IL-1β, IL-18 and TNF-α contents were significantly increased, in ATDC5 cells after miR-3620-5p and miR-6511b-3p inhibition. CONCLUSION: Thus, miR-3620-5p and miR-6511b-3p might be the key effectors in IDD progression by mediating the expression of CPNE6 and B3GAT1 in NP tissues. This newly discovered specific miRNA‑mRNA interactions were identified and validated using our original patient samples, with public datasets used for bioinformatic cross‑validation. It holds huge potential applications for miRNA-based therapies in early diagnosis and treatment of IDD. - Source: PubMed
Publication date: 2026/04/21
Wang JiagangZhu LifanWeng FengbiaoZeng JincaiXu LiangChen YuweiShi Yuhui - N-glycans are essential components of glycoproteins, influencing their properties and functions. While biochemical pathways of glycosylation are well-characterized, their genetic regulation remains poorly understood. This study utilizes matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-MS) and ultra-high performance liquid chromatography-fluorescence detection (UHPLC-FD) to strengthen replication and further characterize previously identified genome-wide association signals for the total human plasma N-glycome (TPNG). Univariate and multivariate genetic association meta-analyses involved 3385 samples across 143 N-glycome traits from the Hoorn Diabetes Care System and DiaGene cohorts as well as 3224 samples across 117 N-glycome traits from TwinsUK, CEDAR, QMDiab and SABRE cohorts. We successfully replicated ten previously identified but not replicated glycosylation quantitative trait loci (glyQTLs) and prioritized five high-confidence putative causal genes, including the glycosyltransferase MGAT4B and inflammation-related genes - C3 and FCGR2B. The linkage-specific sialic acid derivatization in MALDI-MS enabled delineation of genetic effects on α2,3- and α2,6-sialylation. Mass spectrometry analysis, triggered and guided by association to a locus containing B3GAT1 glucuronosyltransferase, provided evidence for hexuronic acid-containing glycans in human blood plasma. These findings advance our understanding of the genetic regulation of protein N-glycosylation and highlight the complementarity of different analytical approaches in glycomics research. - Source: PubMed
Timoshchuk AnnaNaber AnnemiekeSlieker RoderickSoplenkova AnnaMaslov Denis EPotapova Nadezhda ANicolardi SimoneElders P J MSijbrands Eric J GSharapov Sodbo't Hart Leen Mvan Hoek MandyWuhrer ManfredAulchenko Yurii S - Mammalian cells are decorated with a large variety of glycans. Although the biosynthetic enzymes for most glycan structures have been identified, it remains unclear how glycan levels are regulated in cells. Recently, some cellular glycans and their biosynthetic enzymes were found to be loaded into a subset of small extracellular vesicles (sEVs) and transferred to recipient cells, suggesting uncharacterized sEV-mediated mechanisms for glycan remodeling. Here, we found that a brain-specific glycan involved in learning and memory, human natural killer-1 (HNK-1), and its major biosynthetic enzyme, GlcAT-P (B3GAT1), are included in sEVs. Size exclusion chromatography and immunoisolation experiments suggested that the sEVs containing GlcAT-P and glycoproteins with HNK-1 are similar in size but distinct from the tetraspanin-rich sEV subtype. We also found that GlcAT-P in the sEVs is a cleaved form and enzymatically active. Incubation of the HNK-1- and GlcAT-P-loaded sEVs rendered recipient cells positive for HNK-1, whereas sEVs containing GlcAT-P but not HNK-1 did not induce HNK-1 expression in the recipient cells, suggesting that the transfer of HNK-1 but not its biosynthetic enzyme is necessary for recipient cells to be positive for HNK-1. Our findings shed light on a non-genetic pathway for increasing the level of a specific neural glycan via sEV-mediated cell-cell communication. - Source: PubMed
Publication date: 2026/01/12
Tokoro YukoKizuka Yasuhiko