Anti-Human CD42b FITC 25 tests
- Known as:
- Antibody toHuman CD42b fluorecein 25 tests
- Catalog number:
- 11-0429-71
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD42b FITC 25 tests
Related genes to: Anti-Human CD42b FITC 25 tests
- Gene:
- GP1BA NIH gene
- Name:
- glycoprotein Ib platelet subunit alpha
- Previous symbol:
- GP1B
- Synonyms:
- CD42b, GPIbalpha
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human CD42b FITC 25 tests
Related articles to: Anti-Human CD42b FITC 25 tests
- : Pancreatic adenocarcinoma (PAAD) is a highly aggressive malignancy with limited treatment options and a poor prognosis. Extracellular vesicles (EVs), which play a central role in intercellular communication, have emerged as promising non-invasive biomarkers for both diagnosis and prognosis. This study aimed to identify EV-related genes, construct a more accurate prognostic model using data from multiple databases, and explore the functional roles of key genes in PAAD. : Four publicly available datasets, PAAD_ExoRbase, TcgaTargetGtex-PAAD, GSE62452_GPL6244, and GSE78229_GPL6244, were analyzed, leading to the identification of 40 differentially expressed EV-related genes. Using the Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression, five prognostic genes, , , , , and , were selected to construct a nomogram model for predicting patient outcomes. Single-cell analysis showed that these five genes were expressed in T-proliferative, malignant, and ductal cells. Analyses of immune cell infiltration and immune checkpoints further supported the model's prognostic performance. The regulatory role of the key gene was validated in an in-house cohort and confirmed through in vitro experiments and RNA sequencing. Furthermore, analyses of conditioned medium, EV isolation and characterization, and endothelial tube formation assays demonstrated that EVs derived from CFPAC-1 cells carrying enhanced PAAD angiogenesis through VEGF/VEGFR signaling. - Source: PubMed
Publication date: 2026/05/01
Ma TianyinGongye XiangdongDongzhi CairangMa ShuxianChai YiboGuo Wing-WaWang QikunTian Ming - Megakaryopoiesis is an elaborate biological process that primarily occurs in the bone marrow. To gain deeper insights into molecular mechanisms driving normal megakaryopoiesis, we utilized an in vitro human megakaryocytic culture system based on mobilized peripheral blood-derived CD34 cells. Following fluorescence-activated cell sorting (FACS) isolation of CD41 and CD41 megakaryocyte (MK) subsets, mature MKs were confirmed through characterization of MK-specific surface markers, ploidy analysis, Giemsa staining, and immunofluorescence. Subsequent bulk RNA sequencing of these distinct populations enabled the identification of differentially expressed genes (DEGs) and enriched pathways. Based on our CD34-derived MK differentiation model, the expression of CD41 was found robustly induced by day 4 and further elevated by day 10. The CD41 population exhibited marked co-expression of CD42b and CD61, a significantly higher proportion of polyploid cells (≥16 N), along with characteristic morphological features of mature MKs, including proplatelet formation, cytoplasmic maturation, and cell size enlargement compared to the CD41 subset. Transcriptomic profiling of these two populations identified 1877 up-regulated and 1817 down-regulated DEGs in CD41 MKs. Protein-protein interaction (PPI) network analysis of the key DEGs revealed hub genes including VWF, PF4V1, SELP, PF4, GP1BA, CD40LG, PPBP, CLEC1B, P2RY12, and THBS1. Functional enrichment underscored the acquisition of migratory, adhesive, and secretory capacities, marked by significant upregulation of platelet activation and wound healing signatures. Pathway analysis further indicated coordinated activation of focal adhesion, cytoskeletal reorganization, glycerolipid metabolism, and neuroactive ligand-receptor interaction during maturation. This study provides an integrative transcriptomic blueprint of human MK maturation and highlights the novel candidate targets for thrombopoiesis. - Source: PubMed
Publication date: 2026/05/15
Zhang ZiyanWang YueLiu Peng - Major depressive disorder (MDD) is a prevalent mental illness, and inflammatory processes are considered a pivotal component of the pathogenesis of MDD. This study aims to identify novel biomarkers associated with the development of MDD and to elucidate the underlying immunological mechanisms. - Source: PubMed
Publication date: 2026/04/30
Wu XinyuZhou ShaomingYang PingChen JiayiLiu HonghuaShi LuZhang Xuehua - Investigating the genetic basis of adaptation to environmental stresses, such as hypoxia, can enhance our understanding of human biology and resilience. High-altitude adaptation provides a valuable model for studying the genetic mechanisms of the hypoxic response. Indeed, most known loci associated with hypoxic adaptation have been identified in indigenous mountain populations; however, research on elite climbers remains limited. In our previous study, we conducted exome sequencing of experienced mountaineers and identified two pathogenic variants in the and genes, both of which are linked to respiratory failure. These findings encouraged this study, which conducted exome sequencing to explore genetic variation in a larger cohort. - Source: PubMed
Maksiutenko Evgeniia MMerkureva Valeriia АBarbitoff Yury AAseev Mikhail VLazareva Tatyana EGlotov Andrey SGlotov Oleg S - To address the forensic diagnostic challenge of distinguishing Anaphylactic Sudden Death (ASD) from Sudden Death from Coronary Heart Disease (SD-CHD), this study established mouse models of Atherosclerosis (AS) and ovalbumin-induced Anaphylaxis (AP). LC-MS/MS-based serum proteomic analysis of Atherosclerosis (AS) and Anaphylaxis (AP) mice identified fibronectin 1 (FN1), platelet glycoprotein Ibα chain (GP1BA), and platelet factor 4 (PF4) as candidate biomarkers. These candidates were validated by parallel reaction monitoring (PRM), enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry (IHC) in a combined AS + AP mouse model and in post-mortem human cardiac and bronchiolar epithelial tissue. In mice, serum FN1, GP1BA, and PF4 levels were significantly elevated in the AS group, whereas only FN1 was markedly downregulated in AP mice. In human tissues, FN1, GP1BA, and PF4 were all upregulated in Sudden death from coronary heart disease (SD-CHD) myocardial samples, with FN1 showing the greatest increase. In airway epithelium, FN1 was upregulated in anaphylactic sudden death (ASD) and anaphylactic sudden death (ASD) with Coronary Atherosclerosis (ASD + CAS) groups, while GP1BA was downregulated. These results indicate that FN1 serves as a key differential mouse serum biomarker, while PF4 and GP1BA aid in Sudden death from coronary heart disease (SD-CHD) diagnosis. Collectively, this multimarker, multilevel framework provides a molecular diagnostic strategy for the forensic identification of complex sudden death. - Source: PubMed
Publication date: 2026/02/25
Fan Zhi-HaoYue Zi-QiLiu Zi-KangJin Zhan-FengZhang Wei-HuaChen He