Anti - Mouse, CD56 (SCLC) Clone 123C3
- Known as:
- Anti - Mouse, CD56 (SCLC) Clone 123C3
- Catalog number:
- 61-0062-5
- Product Quantity:
- 0.5mL
- 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
- Alzheimer's disease (AD), a neurodegenerative disease primarily affecting older adults, is characterized by changes in memory, behavior, and language. Although gene expression varies during AD progression, the molecular mechanisms underlying this variation remain unclear. RNA sequencing indicates that most genes exhibit minimal gene-level differential expression in AD but may relate to neuronal function. Our comprehensive analysis revealed that neural cell adhesion molecule 1 (NCAM1) underwent alternative splicing (AS) in AD. Notably, an isoform switch occurred from the long isoform (L-NCAM1), typical under normal conditions, to the short isoform (S-NCAM1) in AD. S-NCAM1 lacked the intracellular domain in L-NCAM1. Additionally, the S-NCAM1-to-L-NCAM1 ratio increased in the hippocampus of amyloid precursor protein ()/PS1 mice compared to wild-type mice. Single-nucleus sequencing determined that this change in NCAM1 isoforms occurred predominantly within reactive astrocytes. Hence, AS may play a key role in AD development, while the L-NCAM1-to-S-NCAM1 ratio could serve as a biomarker. - Source: PubMed
Publication date: 2026/03/26
Li HaotianLiu SaiMiao DaoxinChen LongSun YuanWang GuangjiZhu ZheyingLi XinuoLu Qiulun - Tourette Syndrome (TS) is a neurodevelopmental disorder marked by motor and vocal tics. Recent evidence highlights the role of neurotrophic factors like glial cell line-derived neurotrophic factor (GDNF), which may play a key role in the pathogenesis and exacerbation of TS. Qufeng Zhidong Recipe (QFZDR), a traditional Chinese herbal formulation, has demonstrated clinical efficacy in the treatment of TS. However, its potential to enhance neurotrophic support and the underlying molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/04/16
Wu XinnanJiang KeyuWu MinZhao XinZhang Xin - 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