Rat Anti-Mouse CD90 Thy-1.2
- Known as:
- Rat Antibody toMouse CD90 Thy-1.2
- Catalog number:
- 128-10061-1
- Product Quantity:
- 500
- Category:
- -
- Supplier:
- Ray Biotech
- Gene target:
- Rat Anti-Mouse CD90 Thy-1.2
Related genes to: Rat Anti-Mouse CD90 Thy-1.2
- 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-1.2
Related articles to: Rat Anti-Mouse CD90 Thy-1.2
- 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
Miceli M CarrieChesmore KevinScripture-Adams DeirdreBarthelemy FlorianLittle IsaiahWang RichardNieves-Rodriguez ShirleyCorona RosarioSteady NicoleYip ArtemisDouine-Barthelemy EmilieNelson StanleyRengarajan SophieNasif DanielaSen Annabel - To investigate the distribution, lineage fate, and reparative function of Thy1 lineage cells in the mouse mandible. - Source: PubMed
Publication date: 2026/04/15
Zhang LinmeiWu WenjingSu Jiansheng - This study determines the phenotypic and functional characteristics that define distinct fibroblast-like synoviocyte (FLS) populations in rheumatoid arthritis (RA) vs psoriatic arthritis (PsA). - Source: PubMed
Publication date: 2026/04/10
Tynan ÓrlaBrugman Aenea A ISmith ConorCanavan MaryO'Rourke Aoife MFloudas AchilleasAnton DumitruWade SiobhánSundanum SoniaFletcher Jean MOrr CarlVeale Douglas JFearon Ursula - The bone marrow (BM) microenvironment plays a crucial role in regulating hematopoiesis, yet the molecular changes associated with aging in humans remain poorly understood. Using single-cell RNA sequencing, we uncovered transcriptional shifts in BM endothelial cells (EC) and mesenchymal stromal cells (MSC) during aging. Aged sinusoidal EC exhibited a prothrombotic phenotype with compromised mitochondrial and vascular function. Additionally, we identified a novel arterial EC subset, emerging in aged individuals, characterized by RAB13 expression and associated with transcriptional regulatory processes. MSC from aged subjects displayed impaired matrix remodeling and epithelial-mesenchymal transition, driven partly by a subpopulation of THY1 profibrotic cells absent in younger individuals. Finally, immunofluorescent imaging and spatial transcriptomics confirmed the presence of these aging-associated cells in BM samples from aged individuals. In summary, this work provides a comprehensive view of the transcriptional landscape, cellular interactions, and spatial organization of aged EC and MSC, offering novel insights and potential targets that could be exploited for preventing age-associated changes in humans. - Source: PubMed
Cenzano ItziarCócera MiguelLopez-Perez Ana RosaCampos-Dopazo LoreaRuiz JavierSancho IgnacioMartin-Uriz Patxi SanAguirre-Ruiz PaulaSarvide SaraiVilas-Zornoza AmaiaRipalda-Cemborain PurificacionAlignani DiegoLopez AitziberBarrios Marta MiñanaAgreda Delia QuilezYe JinLehmann RobertSudupe LauraAbengozar-Muela MartaLopez-Janeiro ÁlvaroTamariz-Amador Luis-EstebanMuiños-López EmmaSaez BorjaTegner JesperCalvo Isabel AGomez-Cabrero DavidProsper Felipe