Anti - Mouse, CD56 (SCLC) Clone 123C3
- Known as:
- Anti - Mouse, CD56 (SCLC) Clone 123C3
- Catalog number:
- 61-0062-2
- Product Quantity:
- 0.2mL
- 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
- The critically endangered Malayan pangolin (Manis javanica) exhibits distinctive physiological adaptations; nevertheless, its molecular mechanisms underlying development and reproduction remain inadequately characterized, thereby impeding effective conservation initiatives. In this study, we conducted a comprehensive transcriptomic analysis of six tissues (intestine, kidney, liver, lung, muscle, and spleen) derived from adult, fetal, and pregnant individuals. The fetal stage demonstrated the greatest abundance of stage-specific genes, which were predominantly enriched in developmental pathways such as epithelial organization and transmembrane signaling. Differential gene expression (DGE) analysis revealed that genes upregulated in adults were primarily associated with metabolic and immune functions, whereas those upregulated in fetuses were linked to developmental processes and cell cycle regulation. Co-expression network analysis identified critical hub genes, including GLDC in adults and NCAM1 in fetuses, that are implicated in stage-specific regulatory mechanisms. Additionally, extensive differential alternative splicing (DAS) events were observed, with exon skipping (SE) representing the most frequent splicing pattern. Integrative analyses suggested that DGE and DAS largely constitute independent regulatory layers; however, a subset of hub genes, such as OBSL1 and TNIP1, exhibited concurrent differential expression and splicing, indicating their potential central roles in coordinating developmental processes. This study presents a detailed transcriptomic atlas of Malayan pangolin development and pregnancy, providing candidate biomarker genes for evaluating reproductive health and developmental status, thereby informing future conservation strategies. - Source: PubMed
Liang XianghuiJia MiaomiaoWang ZhiguangDing YuShanHou FanghuiXiang ChengweiHuang WanheWang HeXu XuelinMao YingjinChen LumanYang GuangdaShen YongyiChen WuShen Xuejuan - Ductular reaction (DR) is a hallmark of biliary atresia (BA), but its underlying mechanisms remain unclear. In this study, we identified an expanded NCAM1EpCAM hepatic progenitor cells (HPCs) as the predominant DR-related cell cluster using single-nucleus RNA sequencing, and NCAM1EpCAM HPC-derived organoids exhibited impaired biliary differentiation in BA. α-synuclein was characterized as the signature gene of this cluster, exhibiting upregulated expression in liver tissues from both human BA and mouse BA models, as well as in the serum of patients with BA. Biliary organoids derived from mouse single cells and human induced pluripotent stem cells (iPSCs) confirmed that α-synuclein accumulation drove aberrant biliary development in both mouse and human organoids, and induced BA-like transcriptomic alterations, characterized by significant enrichment of the glutathione (GSH) metabolic pathway. Consistently, hepatic GSH was reduced in both human BA and mouse BA models. In human intrahepatic biliary epithelial cells (HiBECs), α-synuclein overexpression decreased cellular GSH content and increased mitochondrial reactive oxygen species (ROS) under oxidative stress. The present study showed that NCAM1EpCAM HPCs were expanded and characterized by an aggregation of α-synuclein in BA, which could increase cellular susceptibility to GSH-associated redox imbalance, and lead to aberrant bile duct regeneration. - Source: PubMed
Publication date: 2026/06/29
Xie HuaZhu MengyanZhu ZhongxianTang JiaqiZhang RuyiDing ZequanLi JunzhiWu ZhongluanTam Paul Kwong HangWang QianghuLui Vincent Chi HangXia YankaiTang Weibing - Prostate cancer remains a major global health concern for men, with hypoxia and immune escape being key drivers of tumor progression; however, no reliable diagnostic signature integrating both processes has been established for clinical use. In this study, we integrated RNA sequencing and microarray data from The Cancer Genome Atlas (TCGA)-PRAD, Genotype-Tissue Expression (GTEx), and Gene Expression Omnibus (GEO) datasets to identify hypoxia and immune escape-related genes (HIERGs). Through differential expression analysis, functional enrichment, and machine learning algorithms including Random Forest, SVM-RFE, and LASSO regression, we constructed a robust six-gene diagnostic signature comprising , , , , , and . The model demonstrated high diagnostic accuracy, with area under the curve (AUC) values exceeding 0.9 across all validation cohorts, as confirmed by calibration curves, decision curve analysis, and receiver operating characteristic curves. Functional analysis revealed significant enrichment in translation-related pathways and smooth muscle contraction, and the RiskScore was significantly associated with altered immune cell infiltration in the tumor microenvironment. Regulatory network analysis further uncovered potential upstream regulators and therapeutic agents targeting the key genes. In conclusion, we developed and validated a hypoxia and immune escape-related gene signature with robust diagnostic performance for prostate cancer. Exploratory grouping by the model-derived RiskScore revealed differences in pathway and immune infiltration patterns, suggesting an association between the signature and intratumoral molecular heterogeneity. These exploratory findings primarily serve to characterize the biological features related to the model and provide supplementary clues for understanding molecular alterations in prostate cancer; they should be interpreted with caution. - Source: PubMed
Publication date: 2026/05/18
Gan HexiaJiang JianaYang JiebinShen FengLu WeihongLai PengChen LingyuXu ZhibingZhang JianpingGuo JianmingChao Fan - Posttraumatic stress disorder (PTSD) is associated with increased risk of chronic disease and premature aging, yet underlying molecular mechanisms remain unclear. We performed plasma proteomics (SomaScan; 9404 proteins) and targeted metabolomics (145 metabolites) in 393 World Trade Center responders (232 with PTSD, 161 trauma-exposed controls). A total of 114 proteins and seven metabolites were differentially expressed in PTSD. Top proteins included NCAN, BCAN, NCAM1, and GDF15. Top metabolites included serotonin, lactate, glutamic acid, and cystathionine. Integrative analyses showed coordinated proteomic-metabolomic alterations, with widespread correlations linking metabolites involved in redox and amino acid metabolism to synaptic and oxidative stress-related proteins. Gene ontology enrichment identified neuronal plasticity, immune activation, extracellular matrix remodeling, and oxidative stress. Proteomic organ aging analyses revealed accelerated aging in the pancreas, lung, and at the organismal level in PTSD. These results reveal a redox-metabolic mechanism through which PTSD may drive multisystem aging and elevate disease risk. - Source: PubMed
Publication date: 2026/06/20
Kuan Pei-FenMann Frank DYang XiaohuaKotov RomanClouston SeanIlkayeva OlgaMuehlbauer MichaelNewgard Christopher BLuft Benjamin J - Autism spectrum disorder (ASD) is highly comorbid with Down syndrome (DS), yet the shared molecular mechanisms remain unclear. DNA methyltransferase 3-like (DNMT3L) is overexpressed in DS brain tissue and plays a role in neural development. However, the neurobiological functions of the heterogeneous nuclear ribonucleoprotein D (HNRNPD) family are still largely unknown. In this study, we generated Drosophila lines that overexpress DNMT3L. Using mass spectrometry, we identified Sqd (Squid), the Drosophila homolog of human HNRNPD, as a binding partner of DNMT3L, and we confirmed their physical interaction. We found that DNMT3L overexpression suppresses Sqd function, increases the mRNA stability of factor of interpulse interval (fipi), and raises its expression level. These changes led to neurobehavioral alterations and altered synaptic plasticity in flies. We further tested this in mammalian cells and confirmed the interaction between DNMT3L and HNRNPD, as well as their regulatory effects on neural cell adhesion molecule 1/2 (NCAM1/2), the mammalian homologs of fipi. Together, our findings reveal a DNMT3L-Sqd/HNRNPD-fipi/NCAM regulatory axis. This work provides a basis for identifying therapeutic targets to treat ASD that occurs alongside DS. - Source: PubMed
Publication date: 2026/06/19
Fan RuonanZhang ZhuoMiao Tingting