Rat Anti-Mouse CD90 Thy-1
- Known as:
- Rat Antibody toMouse CD90 Thy-1
- Catalog number:
- 128-10059-1
- Product Quantity:
- 500
- 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
- The α-synuclein (aSyn) pathology is a predominant feature of synucleinopathies such as Parkinson's disease (PD). Triggers that may induce aSyn aggregation are not completely understood, but include post-translational modifications. One such modification is aSyn truncation exposing the N-terminal glutamine 79 residue that is subsequently converted into pyroglutamate (pE). The pE79-aSyn variant is prone to oligomerisation and thus highly neurotoxic. Here, we used a Thy1-aSyn PD mouse model overexpressing human wild type aSyn to reveal a possible spatial association of aSyn with matrix metalloproteinase-9 (MMP-9) as aSyn-truncating and with isoglutaminyl cyclase (isoQC) as pE-forming enzymes, respectively. We observed a cellular co-localisation of pE79-aSyn with MMP-9 and isoQC in aSyn overexpressing neurons in the substantia nigra. In addition, MMP-9 and GFAP protein expression increased during aging of Thy1-aSyn mice, whereas that of isoQC was reduced. In order to reveal potential cross-disease mechanisms of pE79-aSyn pathology, its cell type-specific appearance and immunohistochemical co-localisation with MMP-9 and isoQC was also evaluated in the tg2576 Alzheimer's disease (AD) mouse model. Here, a different cellular expression pattern with substantial co-localisation of pE79-aSyn with MMP-9, isoQC, QC and aSyn predominantly in amyloid plaque-surrounding astrocytes was detected. Together, these data indicate that the same enzymatic activities, MMP-9 and isoQC, might be involved in the subsequent pE79-aSyn generation in PD and AD mouse models. The cellular origins, however, differ between the mouse models with neuronal expression of aSyn and its modifying enzymes in the PD mouse model and astrocytic expression in the AD mouse model. - Source: PubMed
Publication date: 2026/09/11
Bluhm AlexandraGroßmann MerleMinister CharlotteSchrempel SarahJoseph Maria AntoniaHolzer MaxSauter ClaudeXiang WeiFeja MalteSchilling StephanSchulze AnjaRichter FranziskaHartlage-Rübsamen MaikeRoßner Steffen - Sleep deprivation (SD) has been increasingly implicated in age-related cognitive decline. However, the mechanisms linking SD duration to progressive disruption of glial homeostasis, synaptic vulnerability, and metabolic dysregulation remain poorly defined. - Source: PubMed
Liu XueyanLin HuilingZhong JianChen XiliWang ZonglinShi MengShi HangZhang HuiChen PingYe Zu-Cheng - Rheumatoid arthritis (RA) is characterized by synovial inflammation, synovial fibroblast (SF) activation, and joint destruction. Activated SFs acquire proliferative and invasive properties and interact with macrophages to maintain the inflammatory microenvironment. However, endogenous factors regulating fibroblast activation and fibroblast-macrophage communication in RA are not fully understood. In this study, we examined the expression of insulin-like growth factor binding protein 5 (IGFBP5) in RA synovium at single-cell resolution and investigated its role in SF activation and macrophage polarization. - Source: PubMed
Publication date: 2026/08/26
Bao LunminWang DaomingWang PingLi XiaoduoZhang HailongWan XiufangYuan RuiXie NanziShi MengtingWu ShuchiYue LongfeiCao Xian'eDai HaibingZheng TingJiang Hongmei - Chronic pulmonary diseases, including cystic fibrosis, chronic obstructive pulmonary disease, and chronic bronchitis, as well as ventilator-associated pneumonia, are characterized by persistent infection of mucus-laden airways. (PA) is a dominant pathogen in these conditions and produces volatile organic compounds (VOCs) that have been proposed as biomarkers of disease exacerbation; however, their immunopathogenic roles remain unclear. We investigated PA-derived VOCs using human bronchial epithelial air-liquid interface cultures and murine models. VOCs exposure significantly increased airway mucin expression and induced a proinflammatory response characterized by M1 macrophage polarization (iNOS), neutrophil recruitment, and expansion of IL-17A-producing Thy1.2 lymphocytes. Functional depletion of macrophages, neutrophils, or IL-17A each attenuated mucin production and goblet cell metaplasia, indicating non-redundant contributions to mucus pathology. , IL-17A neutralization partially restored FOXA2 expression and reduced mucin production, supporting a role in mucus regulation. On the mechanistic level, we discovered an IL-17A-dependent dual-axis pathway involving both epithelial cell-mediated autocrine and lymphocyte-mediated paracrine signaling that contributes to the feed-forward loop of inflammation and enhances the signaling pathways regulating mucus hypersecretion in airways. We conclude that PA VOCs activate multiple proinflammatory responses to convergently drive mucus pathogenesis in the diseased lung. - Source: PubMed
Publication date: 2026/08/26
Kuo Shanny HsuanSharma JaishreeWu CongVieson Miranda DKosmider BeataRandell Scott HNanjappa Som GLau Gee W - Primary cultures from fetal or postnatal rodent brain are widely used to study alpha-synuclein (aSyn)-associated mechanisms but poorly reflect age-dependent neurodegenerative processes. We established primary whole-brain cultures from adult Thy1-aSyn (Line 61) mice overexpressing human aSyn and compared them with postnatal and wild-type cultures. Cultures were maintained for 21 days and characterized by electrophysiology, immunohistochemistry, gene expression analysis, and protein biochemistry. Adult and postnatal cultures contained all major neural cell types, including neurons, microglia, astrocytes, and oligodendrocytes. ASyn overexpression was associated with reduced neuronal viability, altered neuronal firing, and increased microglial reactivity. Importantly, adult cultures retained the microgliosis observed in vivo in Thy1-aSyn mice. These findings establish adult Thy1-aSyn whole-brain cultures as a disease-relevant in vitro model for investigating aSyn-associated neuronal dysfunction, neuroinflammation, and cell-cell interactions and for evaluating therapeutic strategies. - Source: PubMed
Publication date: 2026/09/08
Zalpanow DanielaMerten AnnikaStelz SonjaOfner AndreaWeiß SandraRichter FranziskaLau KristinaKotzur Rebecca