CD56
- Known as:
- CD56
- Catalog number:
- 1F-231-T100
- Product Quantity:
- 100 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
- 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 - How fibroblast heterogeneity orchestrates tissue regeneration by remodeling tissue mechanical properties that guide stem cell function is not well understood. Although fibroblasts are increasingly recognized as key regulators of tissue homeostasis, the specific subpopulations and molecular pathways through which they remodel the mechanical niche during hair follicle regeneration are not fully defined. Here, we identify that Hmmr fibroblasts located beneath the dermal papilla (DP) of the hair follicle promote hair follicle regeneration by secreting extracellular matrix (ECM) components to activate hair follicle stem cells. Single-cell RNA-sequencing and immunostaining mapped spatially distinct fibroblast subpopulations in the dermal microenvironment and showed that regional ECM viscoelastic remodeling occurs prior to hair regeneration and coincides precisely with the emergence of Hmmr fibroblasts. Functional studies in vivo and in skin organoids demonstrate that Hmmr fibroblasts act as mechanical sensors that engage DP cells via NCAM1-FGFR1 signaling to stimulate hair regeneration. We propose a tripartite biomechanical module comprising ECM viscoelastic remodeling (effector), Hmmr fibroblasts (sensor), and DP cells (executor) that cooperatively drives hair regeneration. Together, our work identifies a heterogeneous fibroblast-defined mechanical niche as a central regulator of tissue renewal, highlighting the role of fibroblast diversity in coordinating regeneration and advancing our understanding of the mechano-molecular basis of tissue repair. - Source: PubMed
Publication date: 2026/09/14
Tang YuchunWang MengyueYe YuanliJiang JingweiHuang WentingZhao YipingXie QiaoliLin JinranXiang XiaoKe DanXu ChunmingLei Mingxing