Anti-Human CD56 (NCAM) PE 25 tests
- Known as:
- Antibody toHuman CD56 (NCAM) PE 25 tests
- Catalog number:
- 12-0567-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD56 (NCAM) 25 tests
Related genes to: Anti-Human CD56 (NCAM) PE 25 tests
- Gene:
- CADM1 NIH gene
- Name:
- cell adhesion molecule 1
- Previous symbol:
- TSLC1, IGSF4
- Synonyms:
- NECL2, ST17, BL2, SYNCAM, IGSF4A, Necl-2, SYNCAM1, RA175
- Chromosome:
- 11q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-11-02
- Date modifiied:
- 2016-10-05
- 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
- 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: Anti-Human CD56 (NCAM) PE 25 tests
Related articles to: Anti-Human CD56 (NCAM) PE 25 tests
- Glioblastoma (GBM) is defined by infiltration of tumor cells throughout the brain, which drives resistance, recurrence and mortality. Although cell-derived hyaluronidases (HYALs) have been collectively implicated in invasion-associated matrix digestion, we were motivated to investigate contributions of specific HYAL isoforms, which execute a diversity of cell-autonomous and matrix-based functions. After mining transcriptomic data sets to confirm isoform-specific patterns of HYAL isoform expression in human GBMs, we experimentally probed contributions of each HYAL isoform to invasion using three-dimensional engineered matrix platforms. While pharmacological HYAL inhibition slowed invasion, an isoform-specific CRISPR interference screen revealed that suppression of several HYALs, primarily , unexpectedly accelerated invasion in human glioma cells. RNA sequencing of -suppressed spheroids revealed depletion of transcripts associated with reactive oxygen species (ROS) and enrichment of transcripts associated with cell adhesion molecules (CAMs). KD GBM cells indeed produce lower levels of ROS and elevated levels of L1 Cell Adhesion Molecule (L1CAM) and Neural Cell Adhesion Molecule 1 (NCAM1). We show that altered L1CAM cleavage and NCAM1 polysialylation contribute to the elevated invasion in KDs. These changes are accompanied by altered glycocalyx density and cell adhesion, suggesting that HYAL1 regulates invasion by sculpting the glycocalyx to modulate engagement of adhesion receptors. - Source: PubMed
Publication date: 2026/08/10
Weldy AnnaAnanth EshaAcosta ChristopherKumar Sanjay - : Irritable bowel syndrome (IBS) may have health implications beyond the gastrointestinal tract, but its association with incident hypertension remains unclear. : We analyzed 355,404 UK Biobank participants without recorded hypertension at baseline using multivariable Cox regression, propensity score matching, and sensitivity analyses addressing early events, baseline medication use and blood pressure, and competing mortality. Bidirectional Mendelian randomization (MR), Bayesian colocalization, and intestinal transcriptomic analyses examined genetic and tissue-level evidence. : During a median follow-up of 14.09 years, IBS was associated with incident hypertension (HR, 1.26; 95% CI, 1.22-1.30). The association persisted after matching (HR, 1.22; 95% CI, 1.16-1.28) and across sensitivity analyses. Forward MR provided suggestive support: the primary inverse-variance weighted estimate was positive but imprecise (OR, 1.18; 95% CI, 0.78-1.77), while weighted median and outlier-corrected analyses showed positive associations. Reverse MR showed no clear association. SuSiE-based colocalization supported shared signals for IBS with diastolic and systolic blood pressure at the locus (PP.H4, 0.903 and 0.890, respectively). Intestinal expression was lower in IBS, and correlated transcriptional programs involved epithelial remodeling, adhesion, and mucosal immune processes. : IBS was associated with increased long-term hypertension risk, with suggestive genetic support and shared susceptibility signals at . These findings support a potential biological link and prioritize for mechanistic investigation. - Source: PubMed
Publication date: 2026/09/13
Li LuyaoZhao ChangyingWang FeiyangZhao QianZhao YanGong ShoupingLi GuoliangLi Jing - Sleep disturbance is a prevalent public health concern associated with cognitive deficits and emotional dysregulation, yet the mechanisms underlying SD-induced hypothalamic dysfunction remain incompletely understood. Here, we found that two weeks of SD induced marked hypothalamic neuroinflammation, accompanied by increased expression of the pro-inflammatory cytokines , , and , as well as the chemokine , together with reduced neuronal markers, including decreased Nissl-body and NeuN cells. Single-nucleus RNA sequencing (snRNA-seq) suggested that inhibitory neurons exhibited prominent transcriptional responses to SD, including enrichment of inflammatory pathways such as TNF and IL-17 signaling and transcriptional programs associated with neuronal dysfunction. Furthermore, SD was also associated with microglial activation and a phenotypic shift toward a disease-associated state, exhibiting enhanced antigen-presenting and pro-inflammatory capacity. Notably, intercellular communication analysis identified the neural cell adhesion molecule 1 (NCAM1)/fibroblast growth factor receptor 1 (FGFR1) signaling axis as a key mediator of crosstalk between microglia and other cell types. In BV2 cells, recombinant NCAM1 attenuated lipopolysaccharide-induced inflammatory responses in an -dependent manner. Consistently, PVN-targeted knockdown in vivo exacerbated SD-associated microglial activation, neuroinflammation, and neuronal injury. Collectively, our findings elucidate a critical protective role for the NCAM1/FGFR1 axis in mitigating SD-induced hypothalamic neuroinflammation and neuronal injury. This highlights this pathway as a candidate mechanism for further therapeutic investigation in sleep-related neurological dysfunction. - Source: PubMed
Publication date: 2026/09/21
Qu YanxiangLi BoYan ShixuanZhang ChuanjieJi GuohuaLi KaiZhao YujieWang ZuoyangLi XiaopengSong BoQu Lina - Age-related decline in learning and memory functions poses significant challenges in an aging society, with epigenetic dysregulation emerging as a key contributor to cognitive deterioration. As the most prevalent internal RNA modification, N6-methyladenosine (m6A) dynamically orchestrates neural transcriptome plasticity through its "writers," "erasers," and "readers," yet its role in aging-associated cognitive impairment remains underexplored. This study employs an integrated epitranscriptomic approach to investigate m6A-mediated regulation in hippocampal aging processes. Through comparative m6A-mRNA epitranscriptomic microarray analysis of senescence-accelerated mouse prone 8 (SAMP8) and senescence-resistant SAMR1 hippocampi, we identified neural cell adhesion molecule 1 (NCAM1) as a key m6A-regulated effector whose decreased expression correlates with accelerated cognitive deterioration. Mechanistically, we revealed that Methyltransferase-like 3 (METTL3)-mediated m6A modification governs mRNA stability through insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) reader protein-dependent mechanisms, forming a regulatory axis that modulates cyclic AMP response element-binding protein (CREB) signaling pathway activity. Remarkably, targeting of this METTL3/IGF2BP1/NCAM1 axis significantly attenuated cognitive deficits in aged SAMP8 mice. Our findings establish an m6A methylation-dependent paradigm for NCAM1-mediated cognitive preservation during aging, uncovering a novel epitranscriptomic layer in age-related neurodegeneration. - Source: PubMed
Publication date: 2026/09/15
Ji GuohuaZhao YujieLiu XuLi XiaopengLu LiangLiang FengjiYuan YanhongDai YuyingLi BoQu YanxiangSong BoQu Lina - Bone loss is a severe and often irreversible complication of anorexia nervosa (AN), yet the genetic mechanisms underlying this comorbidity remain underexplored. This study focuses on constructing a comprehensive genetic architecture between AN and estimated calcaneal bone mineral density (eBMD). - Source: PubMed
Publication date: 2026/09/17
Han TaoWang YukeDang YixiongXiang RongZeng YanHe ShengJu YeChen ZilanLiu TingLi ZihaoPang YuqiTan WanyiXu JueJiang JingwenJiang Xia