PTPRC Antibody
- Known as:
- PTPRC Antibody
- Catalog number:
- XW-7814
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- PTPRC Antibody
Related genes to: PTPRC Antibody
- Gene:
- PTPRC NIH gene
- Name:
- protein tyrosine phosphatase receptor type C
- Previous symbol:
- CD45
- Synonyms:
- LCA, T200, GP180
- Chromosome:
- 1q31.3-q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: PTPRC Antibody
Related articles to: PTPRC Antibody
- Cardiac fibrosis is a defining pathological feature of diabetic cardiomyopathy (DCM), and excessive activation of cardiac fibroblasts plays a critical role in regulating cardiomyocyte function through paracrine signaling. CCN1 (cellular communication network factor 1), an extracellular matrix protein involved in intercellular communication, has been suggested to influence cardiac remodeling, although its specific impact on cardiomyocytes in DCM has remained unclear. In this study, we found that CCN1 expression was markedly elevated in cardiac tissues from DCM mouse models and in insulin-resistant cell models, with fibroblasts serving as the primary source. Proteomic analysis and co-culture experiments demonstrated that CCN1 suppressed cardiomyocyte macroautophagy/autophagy. To determine its role in vivo, we generated fibroblast-specific knockout mice and established a DCM model, demonstrating that deletion ameliorated cardiac dysfunction and restored autophagic activity. We further identified ITGAV-ITGB1/integrin αvβ1 as the receptor mediating CCN1 signaling in cardiomyocytes. Molecular dynamics simulations and co-immunoprecipitation experiments confirmed that CCN1 engaged ITGAV-ITGB1/integrin αvβ1 through its cysteine-knot-containing (CT) domain. Mechanistically, this interaction activated the downstream PTK2/FAK-MTOR signaling pathway, leading to inhibition of cardiomyocyte autophagy. Together, these findings reveal a previously unrecognized fibroblast-cardiomyocyte signaling axis in which fibroblast-derived CCN1 drives DCM progression by suppressing autophagy through ITGAV-ITGB1/integrin αvβ1-dependent signaling. This work provides mechanistic insight into the pathogenesis of DCM and identifies CCN1 as a potential therapeutic target for mitigating disease onset and progression.: AAV9: adeno-associated virus serotype 9; ADGRE1/EMR1/F4/80: adhesion G protein-coupled receptor E1; BafA1: bafilomycin A; BSA: bovine serum albumin; C8: compound 8; CCN1: cellular communication network factor 1; CF: cardiac fibroblast; CSA: cross-sectional area; DCM: diabetic cardiomyopathy; EIF4EBP1: eukaryotic translation initiation factor 4E binding protein 1; ELISA: enzyme-linked immunosorbent assay; HE: hematoxylin and eosin; HFD: high-fat diet; HG: high glucose; IR: insulin resistance; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MD: molecular dynamics; MTOR: mechanistic target of rapamycin kinase; NRCM: neonatal rat cardiomyocyte; PDGFRA: platelet derived growth factor receptor alpha; PECAM1/CD31: platelet and endothelial cell adhesion molecule 1; PTK2/FAK: protein tyrosine kinase 2; PTPRC/CD45: protein tyrosine phosphatase receptor type C; RPS6KB1: ribosomal protein S6 kinase B1; S100A4/FSP1: S100 calcium binding protein A4; SQSTM1/p62: sequestosome 1; STZ: streptozotocin; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling; WGA: wheat germ agglutinin. - Source: PubMed
Publication date: 2026/05/07
Hu Bo-AngZhang LeiSong MingKong Yan-RuJiao Ya-QiongJia XuZhu PingLi Yu-LinTi YunZhang WeiWang Zhi-HaoZhong Ming - Osteoarthritis (OA) is widely recognized as the most prevalent degenerative disorder affecting the joints, representing a major contributor to chronic pain and disability. Despite its high burden, the molecular mechanisms underlying OA pathogenesis remain poorly understood, particularly in the context of immune microenvironment modulation. This study explores the immune-related OA progression mechanisms and investigates potential biomarkers to aid diagnosis and therapeutic intervention. - Source: PubMed
Publication date: 2026/04/13
Zhang ZhengyaoWang YilinTan ZhiwenYu XiaohuiLiu Bo - The absence of accessible and reliable biomarkers constitutes a critical barrier for the early diagnosis and stratification of neurodegenerative diseases. While peripheral blood offers a minimally invasive window into systemic pathophysiology, identifying molecular signatures that survive biological heterogeneity and technical noise remains an unresolved challenge. In this study, this issue was addressed through a comparative systemic transcriptomic analysis of Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease (AD), and Parkinson’s disease (PD) in whole blood, implementing a comprehensive workflow integrating unsupervised network analysis and supervised machine-learning methods. By employing LASSO regression and cross-validation across independent external cohorts, a stable and specific transcriptomic signature for ALS was identified, comprising key crosstalk genes involved in systemic immune dysregulation and microglial function, including , and . In contrast, AD and PD exhibited weak transcriptomic signatures with poor predictive reproducibility, suggesting a distinctive systemic pathology in ALS. In addition, the study confirms the superiority of linear modeling for this genomic signature: while complex non-linear algorithms, specifically Radial Basis Function (RBF) kernel Support Vector Machine (SVM) and Random Forest, displayed high initial performance, they collapsed due to overfitting during external validation. Conversely, the linear LASSO model demonstrated superior robustness and generalizability (AUC 0.74). In conclusion, this study not only defines a unique systemic immunotranscriptomic signature for ALS, distinguishable from other neurodegenerative pathologies, but also establishes interpretability and linear simplicity as essential factors for developing reproducible blood-based biomarkers with clinical translational potential. - Source: PubMed
Publication date: 2026/04/29
Gascón ElisaCalvo Ana CristinaZaragoza PilarOsta Rosario - γδ T cells boost inflammatory responses and exacerbate tissue damage after ischemic stroke. However, the origin, dynamics, and tissue adaptation of γδ T cells in the ischemic brain and its border regions remain poorly understood. A systematic integration of large-scale datasets is urgently needed. Here, we investigated the impact of ischemic stroke on the state of meningeal and brain-infiltrating γδ T cells and explored their potential contributions to post-stroke inflammation. - Source: PubMed
Publication date: 2026/04/09
Zha MingmingJander AlinaCai HaodiPiepke MariusDegenhardt KarolineWinter LeoMagnus TimGelderblom Mathias - Diabetic kidney disease (DKD) is a common diabetes complication that increases global morbidity and mortality. To identify DKD biomarkers and explore autophagy-related mechanisms to find potential therapeutic targets for DKD treatment. - Source: PubMed
Wang QinLi XiaoqiYe WenWang QiBi Xianjin