NCAM2_MOUSE Ncam2 ELISA tesk kit
- Known as:
- NCAM2_MOUSE Ncam2 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15904
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- NCAM2_MOUSE Ncam2 ELISA tesk kit
Related genes to: NCAM2_MOUSE Ncam2 ELISA tesk kit
- Gene:
- NCAM2 NIH gene
- Name:
- neural cell adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- NCAM21, MGC51008
- Chromosome:
- 21q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-04-25
- Date modifiied:
- 2016-10-05
Related products to: NCAM2_MOUSE Ncam2 ELISA tesk kit
Related articles to: NCAM2_MOUSE Ncam2 ELISA tesk kit
- Alzheimer's disease (AD), the most common cause of dementia, is characterized by progressive memory and cognitive decline. Conventional genome-wide association studies (GWAS) comparing AD cases and controls may miss genetic influences that act along a continuum of cognitive function. Using data from 3007 participants in the National Institute on Aging Late-Onset Alzheimer's Disease Family Study (NIA-LOAD GWAS), we conducted a family-based GWAS of eight quantitative cognitive phenotypes encompassing episodic memory (Logical Memory IA and IIA), working memory (Digit Span Forward, Backward, and Ordering), and semantic fluency (Animal, Fruit and Vegetable, and Vegetable Fluency). Family-based association testing in PLINK v1.9 identified numerous single nucleotide polymorphisms (SNPs) associated with cognitive phenotypes at genome-wide significant ( < 5 × 10) levels. Notably, genome-wide significant variants with cognatic functions were localized to genes implicated in synaptic function, neurodevelopment, and neurodegeneration, including (rs2075650), (rs1521543), (rs12281267, rs959354), (rs1353983, rs970347, rs1392511), (rs2826728), (rs6788201), (rs2988003, rs2381595), (rs16875655), and (rs1937957). Furthermore, the (rs2075650) was significantly associated with AD as a binary outcome ( = 4.60 × 10) and (rs12281267, rs959354), (rs405509), (rs1353983, rs970347, rs1392511) were associated with AD ( < 0.001). Additionally, several pathways including the signaling pathway (adjusted = 2.82 × 10), driven by , , and may contribute to cognitive impairments. This study provides a comprehensive resource of cognitive endophenotype associations in AD families, advancing understanding of the genetic architecture underlying memory, executive function, and cognitive aging, and highlights new therapeutic targets for replication and functional follow-up. - Source: PubMed
Publication date: 2026/04/24
Wang KeshengYang XueyingMagwood GayenellXu ChunNavia R OsvaldoNeils-Strunjas JeanLi Xiaoming - Despite its strong regenerative capacity, liver aging paradoxically increases susceptibility to fibrosis and metabolic dysfunction-associated steatotic liver disease through dysregulated inflammation, senescence-associated secretory phenotypes, and immune-metabolic crosstalk. To systematically characterize these processes, we integrated longitudinal transcriptomics, single-cell RNA sequencing, and machine-learning approaches. We identified 252 aging-associated genes and developed an Aging Gene Score (AGS) to quantify senescence burden across hepatic cell populations. Single-cell analysis revealed macrophages as key drivers of fibrosis progression, with high-AGS myeloid subsets markedly expanded in cirrhotic livers. Using combined Boruta and LASSO algorithms, we established a five-gene biomarker panel (EFEMP1, LUM, DKK3, GPRC5B, NCAM2) that accurately predicts advanced fibrosis (AUC > 0.77). Furthermore, a network pharmacology framework was applied to screen medicine-food homology (MFH) herbs, identifying Fagopyrum dibotrys (Jinqiaomai) and Astragalus membranaceus (Huangqi) as top candidates. Molecular docking demonstrated strong binding between the bioactive compound MOL000098 and the fibrosis-related target COL3A1. Functional assays showed that Jinqiaomai-containing serum alleviates oxidative stress, improves HepG2 cell viability, reduces ALT and AST levels, and suppresses macrophage lipid accumulation, accompanied by reduced expression of inflammatory and fibrosis-related markers. Collectively, our findings highlight macrophage-centered mechanisms linking liver aging and fibrosis and suggest MFH-derived compounds as promising anti-aging and anti-fibrotic dietary interventions. - Source: PubMed
Publication date: 2026/05/26
Xu YingqiLi MaohaoZhu LunLuo YawenSheng WanluJia PanleiSuo RinaBao Lidao - Alzheimer's disease (AD) is characterized by progressive neurodegeneration driven by tau and amyloid-β (Aβ) pathology, although the underlying molecular mechanisms remain incompletely understood. Emerging evidence implicates altered DNA methylation (DNAm) in AD but comprehensive analyses in experimental models are limited. Here, we profile DNAm dynamics in two widely used transgenic mouse models of tau (rTg4510) and Aβ (J20) neuropathology, focusing on the entorhinal cortex and hippocampus. Using reduced representation bisulfite sequencing (RRBS) and methylation arrays across multiple disease stages, we identified widespread pathology-associated DNAm alterations in both models. Tau pathology in rTg4510 mice was associated with extensive DNAm remodeling at genes involved in neuronal plasticity, apoptosis, and lipid metabolism, including , , and . In contrast, J20 mice exhibited more modest changes, primarily at immune-related loci such as , , and . Tau-associated DNAm changes were more consistent across brain areas than those associated with Aβ pathology. Comparison with human AD DNAm datasets revealed overlapping DNAm differences, including hypermethylation at and in rTg4510 mice. These findings provide robust evidence for early, pathology-associated epigenetic alterations in AD and highlight the utility of epigenomic profiling in transgenic models for identifying novel targets for early intervention in AD. - Source: PubMed
Publication date: 2026/04/07
Leung Szi KayWalker Emma MPolicicchio StefaniaDahir AishaVellame Dorothea SeilerSmith Adam RSwarbrick RhianLunnon KatieDempster Emma LAhmed ZeshanHannon EilisCastanho IsabelMill Jonathan - The overall incidence of extramedullary disease (EMD) in acute myeloid leukemia (AML) ranges from 2% to 30.5%, and is potentially associated with short overall survival. However, the risk factors for EMD and the underlying molecular mechanisms remain poorly understood. Here, we analyzed a cohort of 118 adult patients with de novo AML, among whom 27 (22.88%) developed EMD in various body sites, with tissue involvement as the most common (16/118 [13.56%]). Mesothelin (MSLN) expression, detectable at both transcript and protein levels, can serve as an independent risk factor for EMD in patients with AML. Multivariate analyses revealed that MSLN positivity at transcript levels (hazard ratio [HR], 3.43; 95% confidence interval [CI], 1.44-8.20; P = .006) and MSLN positivity on leukemic blasts detected by flow cytometry (HR, 3.28; 95% CI, 1.37-7.86; P = .008) are independently correlated with EMD risk. Mechanistically, MSLN overexpression promotes cell proliferation, metastasis, and invasion in AML cells. MSLN greatly facilitates cell-cell adhesion by binding with mucin 16 (MUC16), resulting in extramedullary dissemination. MSLN also activates the phosphoinositide 3-kinase (PI3K) signaling pathway and upregulates neural cell adhesion molecules (CAMs) CD56 and neural cell adhesion molecule 2 (NCAM2) through interaction with MUC16. Our study highlights the importance of MSLN expression, particularly identified by flow cytometry, as an independent risk factor for EMD in patients with AML, and elucidates its role in modulating PI3K signaling and CAMs in AML cells. - Source: PubMed
Wang LanZhan QianLuo JingLi JuHe ChaocanZhu YanPei CaixiaChen YutingTang Na-NaYin JiaxiuSu LiChen JiaojiaoXie MinglingLiu LinLuo Xiao-Hua - This study aimed to identify plasma proteins causally associated with pulmonary arterial hypertension (PAH) by using a proteome-wide Mendelian randomization (PWMR) approach. We integrated two large proteomic genome-wide association study (GWAS) data sets with two PAH GWAS data sets and applied PWMR, Bayesian colocalization, and SMR to prioritize candidate proteins. Drug prediction, molecular docking, single-cell RNA sequencing (scRNA-seq) profiling, and a phenome-wide association study (PheWAS) were further used to assess druggability and potential phenotypic associations. PWMR identified 271 PAH-associated proteins, which were refined to the following three targets: CASP10, NOTCH3, and NCAM2. Molecular docking showed strong predicted binding between CASP10 and usnic acid and masoprocol and between NOTCH3 and 2-mercaptobenzothiazole. scRNA-seq data revealed CASP10 expression in endothelial and inflammatory cells and NOTCH3 expression in smooth muscle cells and fibroblasts. The PheWAS did not detect any adverse associations that survived the false discovery rate (FDR) correction. Overall, this integrated analysis highlights CASP10 and NOTCH3 as potential therapeutic targets for PAH. CASP10, as supported by stronger predicted druggability and multiomics evidence, warrants priority for further experimental evaluation. - Source: PubMed
Publication date: 2026/03/03
Chen HuaningChen JintongHou ChengchengRui HongbingXie Liangdi