Rat Anti-Mouse CD90 Thy-1
- Known as:
- Rat Antibody toMouse CD90 Thy-1
- Catalog number:
- 128-10059-2
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD90 Thy-1
Related genes to: Rat Anti-Mouse CD90 Thy-1
- Gene:
- THY1 NIH gene
- Name:
- Thy-1 cell surface antigen
- Previous symbol:
- -
- Synonyms:
- CD90
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-07-22
Related products to: Rat Anti-Mouse CD90 Thy-1
Related articles to: Rat Anti-Mouse CD90 Thy-1
- Human pluripotent stem cell (hPSC)-derived retinal organoids provide an in vitro system for generating retinal ganglion cells (RGCs), yet the cellular composition and developmental fidelity of RGC-enriched cultures remain insufficiently characterised. Here, we tested an RGC-enriched approach involving dissociation of hPSC-derived retinal organoids at day 40, corresponding to peak expression of RGC markers, followed by two-dimensional culture conditions intended to enrich for RGC survival. Flow cytometry was used to assess the expression of RGC markers, including POU4F, ISL1, SNCG, and THY1. Across four samples, POU4F expression ranged from 79-95%, ISL1 from 18-58%, SNCG from 22-91% and THY1 from 3-29%, indicating substantial variability between markers and samples. Single-cell RNA sequencing analysis of 73,642 cells identified multiple retinal lineages, including retinal progenitors, RGCs, photoreceptor-committed cells, amacrine and horizontal cells, and retinal pigment epithelium (RPE), as well as off-target populations comprising HOX-enriched posterior neural cells and other cell types. Cellular composition varied across samples. Transcriptomically defined RGCs accounted for 19-45% of cells across samples, with different RGC subclusters identified. These findings indicate that marker-based assessments alone may overestimate RGC identity and reveal substantial cellular heterogeneity, including partially specified RGC states and off-target populations. Accordingly, the term "RGC-enriched" is used in a relative sense based on comparison with previously published scRNA-seq-validated differentiation studies rather than indicating complete lineage purity. Interpretation of RGC enrichment should consider differences between protein- and transcript-based measurements, sampling variability between assays, and the incomplete specification of functional RGC subtypes. - Source: PubMed
Publication date: 2026/04/30
Ma Jessica Yuen WuenVargas-Landin Dulce BGrainok JanyaPébay Alice - Genetically encoded calcium indicators such as GCaMP enable us to monitor neuronal activities from living animals at synaptic levels as well as at whole-brain levels. However, the genetic variation of GCaMP transgenic rats is limited compared with the various demands for neuroscience studies on rats. - Source: PubMed
Tohmi ManavuNamba HisaakiKawamura MeikoHishida RyuichiIguchi ShotaKobayashi KazutoMatsushita NatsukiMashimo TomojiNatsume RieSakimura KenjiNawa Hiroyuki - Muscle fibrosis is a key pathological feature of Duchenne muscular dystrophy (DMD) and is closely associated with disease progression. Fibroadipogenic progenitors (FAPs) are major contributors to fibrosis, yet the precise mechanisms remain unclear. To investigate FAP dynamics and lineage specification, we generated dual-reporter mice (PRURD2) by crossing D2.B10-Dmdmdx/J (D2-mdx) mice with FAP and brown/beige adipose tissue (BAT) reporter lines. Corresponding control mice (PRURDBA) were established on the DBA/2J background. At 12 months, heart, diaphragm, and tibialis anterior (TA) muscles were collected for histological analysis. FAPs were isolated via FACS and subjected to single-cell RNA sequencing. PRURD2 mice exhibited increased fibrosis across all muscles compared to controls ( < 0.01) and a significant rise in PDGFRα-GFP + FAPs ( < 0.05). UMAP clustering identified 11 distinct FAP subpopulations, with the fibrosis-associated CD55 cluster enriched in PRURD2 mice. Pseudotime analysis showed lineage progression from progenitor clusters toward the fibrogenic CD55 cluster. CellChat analysis indicated increased interactions in PRURD2 mice involving fibrosis-related pathways like COLLAGEN, TGF-β, WNT, NOTCH, and ANGPTL. Additionally, fibrosis-related signaling pathways such as THY1, TWEAK, EPHA, EPHB, and SEMA6 showed increased interactions among FAP clusters in PRURD2 mice. Differential gene expression analysis revealed top upregulated genes including , , and . PRURD2 mice develop severe fibrosis in skeletal and cardiac muscle, driven by FAP-induced signaling pathways and genes. This model is valuable for understanding muscle fibrosis in DMD and developing anti-fibrotic therapies. - Source: PubMed
Publication date: 2026/04/24
Fusagawa HiroyoriLau JustinSharma SankalpLiu MengyaoSamimi YusefFranchet-Schaer GabrielFang AshleyFusagawa MinamiKim HubertFeeley Brian TLiu Xuhui - Cuproptosis, a newly identified form of programmed cell death, inhibits liver fibrosis in hepatic stellate cells. However, how cuproptosis influences liver fibrosis in other cells remains to be determined. We aimed to develop a diagnostic model for cuproptosis and to further investigate its role in liver fibrosis. We obtained datasets of patients with metabolic dysfunction-associated fatty liver disease from the Gene Expression Omnibus. A diagnostic model was established using WGCNA and machine learning, and the model demonstrated a satisfied accuracy in the training and validation sets. Single-cell RNA (scRNA) confirmed that cuproptosis is highly likely to occur in hepatocytes and likely promotes liver fibrosis through communication with macrophages and dendritic cells. Immunohistochemistry analyses revealed that THY1 localized to fibroblast membranes and SMOC2 localized to hepatocytes. Molecular docking and molecular dynamics were used to identify the most suitable therapeutic drugs and suggested that breviscapine may target THY1, which may have a therapeutic effect on liver fibrosis. These findings establish a diagnostic model based on cuproptosis-related genes for liver fibrosis, identify THY1 and SMOC2 as key diagnostic biomarkers, and propose a model in which the expression of these markers in hepatocyte are associated with fibrosis progression, potentially through immune-mediated mechanisms. - Source: PubMed
Gao RanyanChen HongliangWang JiaxinXu LingyiLi FengchunJiang XinyuGeng XinyuLi NingChaulagain Ram PrasadDeborah Oluwaseun BabalolaLi WanweiJin Shizhu - Single cell/nuclei technologies have revolutionized our understanding of the remodeling of complex multi-cellular tissue that accompanies injury, regeneration, and disease. Duchenne muscular dystrophy (DMD) is a fatal genetic disease of childhood characterized by progressive skeletal muscle weakness resulting from mutation of DMD and loss of functional dystrophin. Here we report, at single nuclei/cell resolution, on intramuscular cell and gene expression dynamics within a broad cohort of needle muscle biopsies obtained from DMD individuals with varying degrees of severity, including a subset with low levels of dystrophin. We report a strong negative correlation between expression of dystrophin and disease severity and report substantial differences in cellularity and cell type-specific gene expression in DMD severity groups versus healthy muscle. Expression signatures indicate that DMD myofibers become immunologically alert, upregulating innate and adaptive immune sensors, including TLR4, IL15, TNF family receptors and MHC and costimulators. In this cohort, dystrophic muscle was remodeled with 50% fewer myofibers with expansion and diversification of fibroblasts and myeloid cells. We identify a DMD-specific TNFα-responsive Thy-1+/C3+ fibroblast subpopulation which we propose are inflammatory tissue priming fibroblasts and three DMD-specific myeloid populations which express signatures of innate immune memory. There is an 8-fold increase in CD8+GZMK+/GZMB+ T cells (Tek), with characteristics of both adaptive and innate immune activity. We propose that these non-myofiber muscle resident cells interact and epigenetically instill long-term tissue memory to perpetuate and amplify a hyper-inflammatory state in DMD muscle, contributing to impaired regeneration, myofiber death and fibrosis. This compendium of single/cell nuclei serves as a valuable reference and has immediate impact for biomarker discovery, clinical trial design, identification of barriers to dystrophin replacement therapies and novel druggable cell mechanisms operating in DMD. - Source: PubMed
Publication date: 2026/04/08
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