Rat Anti-Mouse CD90 Thy-1.2
- Known as:
- Rat Antibody toMouse CD90 Thy-1.2
- Catalog number:
- 128-10061-2
- Product Quantity:
- 1 mg
- 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
- Vascular plasticity is a crucial biological asset enabling our bodies to rapidly adapt to infections and acute inflammation. However, repeated insults during chronic disease can result in these vascular adaptations becoming irreversible, thereby driving disease progression and fibrosis. This study aimed to understand if phenotypic changes in endothelial cell (EC) identity could be indicative of progressive fibrosis and thereby offer diagnostic and therapeutic opportunities for patients with metabolic dysfunction-associated steatotic liver disease (MASLD). We integrated high-resolution imaging, proteomic and transcriptomic analysis which collectively highlighted a central role for endothelial-to-mesenchymal transition (EndMT)-induced EC plasticity in the derivation of 'fibrosis-associated' EC (FAEC). We demonstrated that: 1) full spectrum flow cytometry can provide new opportunities to categorize and phenotype EC subpopulations, 2) two distinct EndMT-derived FAEC subpopulations expanded during fibrogenesis; THY1.2+ICAM1+ and TAGLN+MCAM+ EC that displayed unique immunomodulatory and metabolic phenotypes, 3) TAGLN+ FAEC are a conserved, pro-fibrotic cell type that arose at early stages of MASLD, and 4) increased hepatic expression of TAGLN was significantly associated with detrimental patient outcomes at all stages of liver disease. This study paves the way for the development of FAEC-specific diagnostic and therapeutic approaches to tackle progressive fibrotic disease. - Source: PubMed
Publication date: 2026/09/01
Gkantsinikoudi ChristinaDignam Joshua PKumar RajuJokl ElliotRana MeenakshiLi WenhaoSamus MarynaLandi StephanieAthwal Varinder SKendall Timothy JRot AntalFallowfield Jonathan APiper Hanley KarenAlazawi WilliamDufton Neil P - The pathobiology of multiple myeloma is influenced by cells of the bone marrow, but whether tumor support is organized in a spatially-defined tumor microenvironment (TME) remains unclear. Using spatial transcriptomics and imaging mass cytometry, we show that myeloma cells initially exist as scattered cells throughout the marrow, yet with disease evolution condense into a spatially-defined TME. Dense tumor nodules contain a cellular ecosystem distinct from the surrounding marrow, enriched for macrophages, conventional dendritic cells, and CD8⁺ T cells, as well as endothelial cells and THY1⁺ mesenchymal stromal cells. Conversely, neutrophil lineage cells are absent from this TME but interact with scattered myeloma cells outside of dense nodules. Presence of the dense tumor architecture at diagnosis confers a worse prognosis, emphasizing the relevance of spatial organization of the bone marrow. Together, these findings define a discrete spatial and cellular myeloma TME, that provides spatially-guided insights into patient stratification and disease pathobiology. - Source: PubMed
Publication date: 2026/09/01
Koops MarnixBertamini LucaPapazian NatalieKorst CharlotteBudai Mátyás JánosHoogenboezem Remco MSanders Mathijs Avan der Holt Bronnovan Duin MarkBroijl AnnemiekBalogh PéterZweegman SonjaRaaijmakers Marc Hgpvan de Donk Niels W C JKellermayer ZoltánSonneveld PieterCupedo Tom - Pulmonary fibrosis (PF) is a progressive and fatal lung disorder driven by abnormal fibroblast activation and excessive extracellular matrix (ECM) deposition, leading to structural and functional decline. Existing therapies can slow progression but fail to interrupt fibrotic remodeling. Here, we engineered HUCMSC-Lipo, an inhalable biomimetic formulation fusing human umbilical cord mesenchymal stem cell (HUCMSC) membranes with artificial phospholipids, with formulation parameters systematically optimized using a Bayesian optimization (BO) framework to ensure structural stability and nebulization compatibility. HUCMSC-Lipo maintained membrane functionality and structural integrity for effective nebulized delivery. We successfully established a non-human primate (NHP) PF model and innovatively developed a multidimensional evaluation framework. Utilizing a range of methods, including but not limited to positron emission tomography/computed tomography (PET/CT) molecular imaging with radiolabeled fibroblast activation protein (FAP) inhibitors, we confirmed that HUCMSC-Lipo suppressed fibrotic progression and restored pulmonary function by targeting the regulation of fibroblast activation. Mechanistically, THY-1 enrichment in HUCMSC-Lipo bound integrin receptors to block the FAK/PI3K signaling cascade and restore fibroblast mechanosensitivity, fundamentally turning off the pathological activation "switch" in fibroblasts. Our work presents an inhalable biomimetic formulation that combines therapeutic efficacy with synthetic accessibility, offering a mechanism-targeted approach to PF treatment with strong clinical translatability. - Source: PubMed
Publication date: 2026/08/04
Zhao FangyuSun YigeWang HaoranHou DayongZhang RuiXia WenjingZhang YongchenLi LuyaoZhao XueqiWang KaiqiPan WenwenWang JiannanWang KaiYang LiliChen WeiLi XinNong ChunyangLu HuiyingZhang YiZhang ZhaoyangWu LinaHan ZhaoguoTang Ben-ZhongSun Xilin - Osteoarthritis (OA) is the most prevalent degenerative joint disease worldwide and imposes a substantial public health burden due to the lack of effective disease-modifying drugs. Exosome-related genes participate in exosome biogenesis, cargo sorting, and secretion, serving as critical regulatory elements in exosome-mediated intercellular communication. However, their systematic characterization in OA and their potential as diagnostic or therapeutic targets remain largely unexplored. We obtained OA and normal control samples from the GEO database. Using exosome-related gene signatures as a filtering strategy, we integrated differential expression analysis, protein-protein interaction network assessment, and machine learning algorithms to screen for key diagnostic genes, and constructed and externally validated diagnostic models and nomograms. Enrichment analysis and immune infiltration assessment were performed to explore biological functions and immune microenvironment features. Cellular experiments were conducted to validate the effects of the prioritized gene THY1 on chondrocyte apoptosis, senescence, mitochondrial function, and cell viability. We successfully identified THY1, FAP, and TIMP4 as independent diagnostic markers for OA and constructed a diagnostic model and nomogram with high applicability, whose reliability was validated in an external validation cohort. Enrichment and immune infiltration analyses preliminarily identified two OA subtypes with distinct immune infiltration profiles. Cellular experiments confirmed that THY1 overexpression promoted chondrocyte senescence and apoptosis under OA-like inflammatory conditions, while impairing mitochondrial function and cell viability. Through bioinformatic screening and in vitro experimental validation, this study reveals the pro-apoptotic and pro-senescent regulatory effects of THY1 on chondrocytes under inflammatory conditions, and establishes a diagnostic model and subtyping framework for OA based on three genes, offering new perspectives for stratified diagnosis and future translational research in OA. - Source: PubMed
Publication date: 2026/08/25
Huang LiangkunWen YaXu HanzheZhang ZePei ZijieZhao PiqianSun Fengpo - The role of histidine metabolism in heart failure (HF), particularly its heterogeneous regulation across cardiac cell types, remains unclear. This study aims to define its mechanistic basis and identify key regulatory genes. - Source: PubMed
Publication date: 2026/08/10
Xiao SonglinMo ChunleiLiu QixingXu Li