Anti - Mouse, CD56 (SCLC) Clone 123C3
- Known as:
- Anti - Mouse, CD56 (SCLC) Clone 123C3
- Catalog number:
- 60-0062
- Product Quantity:
- 6 mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse CD56 (SCLC) Clone 123C3
Related genes to: Anti - Mouse, CD56 (SCLC) Clone 123C3
- Gene:
- NCAM1 NIH gene
- Name:
- neural cell adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- NCAM, CD56
- Chromosome:
- 11q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: Anti - Mouse, CD56 (SCLC) Clone 123C3
Related articles to: Anti - Mouse, CD56 (SCLC) Clone 123C3
- ObjectiveGastroblastoma is a rare biphasic neoplasm. This study aims to explore its clinicopathological features, immunophenotype, and molecular genetic alterations to enhance understanding and prevent misdiagnosis.MethodsWe retrospectively analyzed an 18-year-old man with gastroblastoma, and relevant literature was reviewed and summarized.ResultsHistologically, the tumor exhibited a distinctive biphasic pattern. The majority of tumor cells were epithelioid, arranged in nests, cords, glands, and rosette-like structures, with eosinophilic secretions within lumina. Focally, spindle-shaped tumor cells were observed. Mitotic figures were rare. Immunohistochemically, epithelioid cells expressed AE1/AE3, CD56 (NCAM1), and partially expressed CD10 (MME). Spindle cells expressed CD10, and CD56. Next-generation sequencing revealed a fusion gene. No recurrence or metastasis was observed during a 17-month postoperative follow-up.ConclusionGastroblastoma is a rare entity that poses diagnostic challenges. Accurate diagnosis relies on integrating histomorphological features with immunohistochemical studies and molecular analysis. Surgical resection is the treatment of choice. - Source: PubMed
Publication date: 2026/04/08
Wu QiLiu Yufei - To investigate the shared molecular mechanisms between Parkinson's disease (PD) and COVID-19 through integrated bioinformatics analysis and single-cell RNA sequencing (scRNA-seq). We conducted a comprehensive analysis of bulk RNA-seq data from publicly available databases, along with scRNA-seq data from brain tissues of COVID-19 patients. Differential expression analysis identified 725 differentially expressed genes (DEGs) in COVID-19 and 633 in PD samples. A total of 77 overlapping DEGs were identified, highlighting common pathways associated with neuroinflammation and dopaminergic neuron dysfunction. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses revealed significant enrichment in inflammation-related pathways. The protein-protein interaction network analysis identified CHI3L1 as a key gene linking PD and COVID-19. ScRNA-seq analysis revealed a significant increase in CHI3L1-expressing astrocytes in COVID-19 samples, indicating a potential mechanism by which COVID-19 may exacerbate PD symptoms. Furthermore, cell-cell communication analysis revealed enhanced interactions between astrocytes and microglia, excitatory neurons, or oligodendrocytes through signaling molecules such as phosphoprotein 1, CADM1, NCAM1, NRG, and NRXN1, suggesting that astrocytes play a central role in regulating neuronal excitability, synaptic plasticity, and immune responses in the context of COVID-19. These findings suggest a complex interplay between COVID-19 and PD, emphasizing the need for further investigation into the shared pathogenic mechanisms and potential therapeutic targets.IMPORTANCEThis study demonstrates the critical role of neuroinflammation and dopaminergic neuron damage in the shared pathogenesis of COVID-19 and Parkinson's disease. CHI3L1 emerges as a key target, highlighting its potential involvement in modulating neuroinflammatory pathways and synaptic plasticity. The functional significance of CHI3L1, along with its pathological relevance, warrants further investigation through larger studies. Additionally, the active intercellular communication among astrocytes, microglia, and excitatory neurons underscores the profound impact of COVID-19 on neural circuitry. Collectively, these results provide important insights into the mechanisms driving the neurodegenerative consequences of COVID-19, emphasizing the need for continued exploration of therapeutic interventions and the long-term neurological effects of viral infection. - Source: PubMed
Publication date: 2026/04/03
Su YangMa HuiNiu JiayuanHou DongnanLi Liya - Islet amyloid polypeptide (IAPP) is a 37-residue peptide hormone copackaged and cosecreted with insulin by pancreatic β-cells. A pathological hallmark of type II diabetes is the self-assembly of IAPP into β-sheet rich amyloid fibers, which is associated with β-cell impairment. Previously, we showed that a cell-penetrating peptide (CPP) construct, consisting of a hydrophobic signal sequence coupled to a polycationic nuclear localization signal (NLS)-like sequence, exhibited potent antiprion activity and antagonism of Alzheimer's disease-associated amyloid-β (Aβ) peptide aggregation and neurotoxicity. Here, we have extended this approach toward type II diabetes by assessing the efficacy of the CPP construct, designated as neural cell adhesion molecule-1 (NCAM1)-prion protein (PrP), in inhibiting IAPP oligomerization, fiber formation, and associated cytotoxicity. Using complementary and experiments, we show that NCAM1-PrP effectively modulates IAPP's toxic structures into nontoxic conformations. This study underlines the potential of our designed CPP-based therapeutic approach as a versatile tool in the battle against amyloid-associated pathologies. - Source: PubMed
Publication date: 2026/04/02
Oh YujeongPalanikumar LHowarth MadelineMaity DebabrataAli LiaqatMustafa MoradKumar SunilHamilton Andrew DMagzoub Mazin - Chronic Kidney Disease (CKD) has emerged as a significant global public health concern, with membranous Nephropathy (MN) being the most prevalent pathological type of nephrotic syndrome in adults. MN is classified as an antibody-mediated autoimmune disease. There is a growing interest in the research of MN-related antigens. Furthermore, the treatment of MN predominantly relies on the administration of immunosuppressants, with traditional regimens such as corticosteroids and cyclophosphamide, which have significant side effects, and rituximab, having a 35-40% failure rate, highlighting the critical need for the development of specific and effective immunotherapy strategies. In this review, we summarized the research progress on newly discovered MN-related antigens, including exostosin 1/exostosin 2(EXT1/EXT2), Neural Cell Adhesion Molecule 1 (NCAM-1), Neural Epidermal Growth Factor-like 1 (NELL-1), Contactin 1 (CNTN1), Semaphorin 3B, High-Temperature Recombinant Protein A1 (HTRA1), protocadherin FAT atypical cadherin 1(FAT1) and Protocadherin 7(PCDH7). Among them, NELL-1 and HTRA1 primarily serve as target antigens for primary MN, and their serum antibody titers show a strong correlation with disease activity. While EXT1/EXT2, NCAM1, CNTN-1, and FAT1 mainly act as target antigens for secondary MN. In addition, we evaluated the clinical applications and efficacy of novel immunosuppressants and therapeutic approaches, including new anti-CD20 antibodies, proteasome inhibitors, anti-plasma cell therapies, belimumab, complement inhibitors, and immunoadsorption. The new anti-CD20 agents represented by obalimumab and obinutuzumab, along with anti-plasma cell therapies such as daratumumab, have emerged as ideal alternatives for patients with rituximab resistance. Other therapeutic approaches, including complement inhibitors, immunoadsorption, and belimumab, have also exhibited their unique advantages. - Source: PubMed
Publication date: 2026/03/31
Sui LuJin ZihangMeng YilinWu HaozeChe LigeerSun Li - Hilar cholangiocarcinoma (HC) is a highly aggressive malignancy with a poor prognosis, highlighting the urgent need to elucidate its molecular drivers. This study aimed to systematically identify and functionally validate key genes and pathways driving HC pathogenesis. RNA sequencing (RNA-seq) was performed on paired primary HC tumors and matched adjacent non-tumorous tissues to identify differentially expressed genes (DEGs). Subsequent bioinformatic analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction (PPI) network construction, were conducted to characterize the functional landscape and identify hub genes. Transwell assays and orthotopic metastatic models were used to investigate the functions of Contactin-1 (CNTN1) in HC invasion in vitro and metastasis in vivo. RNA-seq analysis identified 35 DEGs in HC, mainly involved in cell adhesion, cytoskeletal regulation, and axon development. PPI network analysis identified six hub genes, including , , , , , and . Furthermore, we demonstrated that CNTN1, a neuronal membrane glycoprotein, was markedly up-regulated in HC at both mRNA and protein levels, and its elevated expression correlated with poor prognosis. Gain- and loss-of-function studies demonstrated that promotes HC cell invasion in vitro and metastasis in vivo. Mechanistically, exerts its pro-invasive effects by activating the PI3K-AKT signaling pathway and inducing epithelial-mesenchymal transition (EMT). Our integrated analysis identifies as a critical oncogenic driver in HC, promoting metastasis through PI3K-AKT-mediated EMT. These findings nominate as a potential prognostic biomarker and therapeutic target in HC. - Source: PubMed
Publication date: 2026/03/11
Ding XiangmingCai ChiyuLu YuanxiangWang ZipengHou JunjingXue YushuZhang LuyunXie MengLi Dongxiao