CD56
- Known as:
- CD56
- Catalog number:
- 1P-231-T025
- Product Quantity:
- 25 tests
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD56
Related genes to: CD56
- 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: CD56
Related articles to: CD56
- : 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 - Overweight and obesity remain global health issues that should not be overlooked. They may impair immune health and alter the function of natural killer (NK) cells, immune effectors that may help regulate immune surveillance and associate metabolic inflammation. Therefore, the present case-control study investigated the immunological profiles of NK cells, both overall and by subpopulations [neural cell adhesion molecule 1 (NCAM1/CD56) staining: Weak (CD56) and strong (CD56)], in 125 Thai participants stratified into five groups by lipid profiles [normal lipid (NL) and dyslipidemia (DL) and body mass index (BMI; normal weight [NW], overweight [OW] and obesity class-I (OB-I)]. NK cells' immunological profiles were determined by flow cytometry. It was found that total NK cell percentages were significantly higher in the DL/OB-I group than in the NL/NW group (P<0.01) and the NL/OW group (P<0.05). Interferon-gamma (IFN-γ)-producing CD56 NK cell percentages were also highest in the DL/OB-I group. BMI correlated positively with total NK cell percentage (R=0.214; P<0.05), CD56 NK cell percentage (R=0.217, P<0.05), and IFN-γ-producing CD56 NK cell percentage (R=0.463; P<0.01). Altogether, the findings demonstrated that NK cell percentage and activation increased markedly with BMI and dyslipidemia. The immunological profiles of NK cells were particularly altered in the DL/OB-I group, characterized by higher percentages and cytokine-producing capacity. Therefore, BMI and lipid profiles must be controlled to preserve immunological status and prevent subsequent low-grade inflammation. - Source: PubMed
Publication date: 2026/08/28
Surapaitoon ArpaFaksri KiatichaiNawawishkarun PunnapatPhanthanawiboon SupraneeJaisiri KingkanSirichoat AuttawitBudmala ParamaNithichanon ArnoneJumnainsong AmonratSalao KaninPhoksawat Wisitsak