Human CD56 ELISA kit (4X96T)
- Known as:
- Human CD56 Enzyme-linked immunosorbent assay test reagent (4X96T)
- Catalog number:
- LF-EK50714
- Product Quantity:
- 4
- Category:
- Elisa Kits
- Supplier:
- Abfron
- Gene target:
- Human CD56 ELISA kit (4X96T)
Related genes to: Human CD56 ELISA kit (4X96T)
- 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: Human CD56 ELISA kit (4X96T)
Related articles to: Human CD56 ELISA kit (4X96T)
- 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 - Cognitive impairment still occurs despite well-controlled HIV but with milder symptoms. People with and without HIV have different neuronal protein changes that may differentiate the asymptomatic neurocognitive impairment (ANI) condition from normal cognition (NPN) and mild neurocognitive disorder (MND). Plasma neuronal-enriched extracellular vesicles (nEVs) were isolated from people with HIV (PWH) with NPN, ANI, or MND, and HIV seronegative controls with NPN (HIV-). Two different platforms were used to delineate protein patterns between sexes and cognitive conditions. When combining results from men and women, the nEV cargo in many cases showed little difference between cognitive conditions. However, when separated, there were different patterns between the sexes for some nEV cargo that distinguished the HIV- groups and HIV+ cognition groups. PWH with NPN had higher nEV toxic proteins compared to individuals without HIV. Women with HIV showed perfect separation between NPN and ANI with Aβ42 and NCAM-1 and perfect separation between ANI and MND with Aβ40 and NCAM-1. Men with HIV with MND had significantly higher NCAM-1 when compared to ANI, and lower GLRX when compared to NPN. This study shows distinct markers for different HIV cognitive categories, many of which differed between men and women. - Source: PubMed
Publication date: 2026/08/31
Tang NorinaXia FanFreasier HeatherTien Phyllis CGlesby Marshall JMerenstein DanielFrench Audrey LMcKay HeatherDiaz Monica MOfotokun IghoLake Jordan EMargolick Joseph BKim Eun-YoungLevine Steven RFischl Margaret ALi WeiMartinson JeremyPulliam Lynn - The COVID-19 pandemic has created a global health challenge. Severe cases are associated with immune system dysfunction, which can lead to uncontrolled inflammation. There are no published data on the specific roles of natural killer (NK)-cell subsets and immune checkpoint (IC) molecules in disease severity. Thirty-five patients diagnosed with COVID-19 and 14 healthy controls were involved in the study. From peripheral blood, CD56dim and CD56bright cell subsets were analyzed by flow cytometry for the expression of IC molecules (T-cell immunoglobulin and ITIM domain [TIGIT], CD226, and PD-1), activation markers (CD69), and cytotoxic potential (CD107a degranulation, granzymes, and perforin content). In COVID-19 patients, the proportion of CD8- CD56dim cells was significantly higher than the CD8+ subset. Inhibitory receptors TIGIT and PD-1 exhibited significantly higher relative expression in CD8+ CD56dim cells compared to their CD8- counterparts across infected groups, an effect particularly pronounced in deceased patients. Conversely, activating CD226 expression was reduced in the CD8- CD56dim subset only in severe cases. Functional assays revealed significantly elevated CD107a and CD69 expression in CD56dim cells of patients versus controls. Notably, CD8- CD56bright cells from deceased patients demonstrated enhanced CD107a expression and elevated perforin content, suggesting a shift toward hyperactivation. The preferential upregulation of inhibitory checkpoint molecules on the highly active CD8+ subset may reflect a compensatory response to immune activation, whereas the enhanced activation of CD8- NK-cell subsets was associated with disease severity and mortality. Similarly, the heightened cytotoxic profile of CD8- CD56bright cells observed in fatal cases may reflect immune dysregulation associated with severe COVID-19. - Source: PubMed
Meggyes MatyasNagy David UToth IldikoMezosi LiviaSipos DavidPeterfalvi AgnesSzereday Laszlo - Neural cell adhesion molecule-1 (NCAM-1), a marker of synaptic plasticity is reported to be altered and associated with cognitive dysfunction in schizophrenia. The aim of the study was to analyse the allele and genotype frequency of neural cell adhesion molecule-1 (NCAM-I) gene polymorphism (rs1836796, rs2303377, rs584427, rs646558) and plasma NCAM-I levels in schizophrenia and their association with cognitive function. Two hundred and sixteen (216) schizophrenia patients and 216 controls were enrolled in the study. NCAM-I polymorphism and its plasma levels were analysed in cases and controls. Cognitive status was evaluated using ACE-III scores. The rs 1836796 genotype was associated with cognitive status (p = 0.011) in schizophrenia. Among the genotypes of rs 1836796, the TT variant (OR: 2.193, 95% CI: 1.097-4.386, p = 0.0292) conferred a potential increased risk of schizophrenia. Attention score (p < 0.05), memory score (p < 0.01), fluency score (p < 0.01), language score (p < 0.01), Visuospatial abilities score (p < 0.01) and total ACE III scores (p < 0.01) were significantly reduced; negative symptom score (p < 0.01), general psychopathological Score (p < 0.01) and total PANSS score (p < 0.01) was significantly increased in TT genotype compared to GG genotype. We conclude that single nucleotide polymorphisms of NCAM-I increase the risk of schizophrenia and are related to severity of the disease and cognitive impairment. - Source: PubMed
Publication date: 2024/12/13
Keshri NehaNandeesha HanumanthappaRajappa MedhaMenon Vikas