NCAM1_MOUSE Ncam1 ELISA tesk kit
- Known as:
- NCAM1_MOUSE Ncam1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15732
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- NCAM1_MOUSE Ncam1 ELISA tesk kit
Related genes to: NCAM1_MOUSE Ncam1 ELISA tesk kit
- 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: NCAM1_MOUSE Ncam1 ELISA tesk kit
Related articles to: NCAM1_MOUSE Ncam1 ELISA tesk kit
- Natural killer (NK) cells contribute to the innate immune system and are pivotal for the defence against opportunistic pathogens, including fungi. (AF), a filamentous mold, can cause invasive pulmonary aspergillosis in immunocompromised patients, e.g. in patients after allogeneic stem cell transplantation (alloSCT). In this pilot study, we challenged NK cell samples from alloSCT recipients collected 90, 120, and 180 days after transplantation and from healthy individuals with AF and characterize the proteome response differences. We identified 2259 differentially abundant proteins between the NK cell proteomes of alloSCT recipients and healthy individuals. Among these, 1118 proteins were differentially abundant at all time points and 1931 proteins specifically at day 180 post-alloSCT. Following stimulation of NK cells with AF, we found a profoundly different early proteome (day 90, =1652 proteins), while at day 180, only 77 proteins remained significantly differentially abundant. We identified, among others, a major differentially abundant protein cluster related to IL27RA (including OAS, STAT1, and MX). Furthermore, for selected markers [granzyme A (GZMA), Neural Cell Adhesion Molecule 1 (NCAM1/CD56), perforin-1 (PRF1)], we confirmed our proteome data by flow cytometry in NK cells from an independent second patient and healthy individual cohort. In conclusion, we demonstrate the advantage of combining comprehensive proteomic profiling with targeted flow cytometry to investigate NK cell responses to AF. Our data analysis connects STAT1 with IL27RA as well as granzyme, IFNg, and NCAM1 activity, which may be exploited towards future therapeutics warranting confirmation in larger study cohorts. - Source: PubMed
Publication date: 2026/05/15
Springer JanDrobny MatthiasHeilig LindaKraus SabrinaKniemeyer OlafKrüger ThomasOlischer ChristianBussemer LydiaPanagiotou GianniBrakhage Axel AEinsele HermannSchäuble SaschaLöffler Jürgen - Oligodendrocytes deposit different amounts of myelin in each neocortical layer, but the regulatory process remains unclear. We present a single-cell map of oligodendrocyte lineage cells purified from different layers of the neocortex across developmental stages. We find that each layer contains a similar compendium of oligodendrocyte classes and differs primarily in the proportions of maturation states, suggesting that oligodendrocyte heterogeneity cannot explain layer-specific myelination. We show that signals from different classes of pyramidal neurons can control oligodendrocyte maturation and the differential distribution of myelin across cortical layers. We generated a ligand-receptor interactome to predict interactions between projection neuron types and oligodendrocyte states, across cortical layers and time, and validated candidates in vivo. We find that neuronal expression of Fgf18, Ncam1, and Rspo3 promotes cortical myelination. This work provides a comprehensive molecular description of oligodendrocyte development in the mouse cortex, pointing to mechanisms whereby neuron-class-linked signals modulate myelin distribution in the neocortex. - Source: PubMed
Publication date: 2026/06/02
Domínguez-Iturza NuriaJokhi VahbizKim KwanhoShetty Ashwin SDi Bella Daniela JPereira Luppi MilagrosYuan WenAbbate CatherineOyler-Castrillo PaulOliver Nalini AVenkat VaishnaviJin XinSimmons SeanLevin Joshua ZBrown Juliana RArlotta Paola - Estrogen receptor-positive breast cancer represents a significant proportion of breast cancer brain metastasis but remains understudied. Here we show that FGFR1-amplification, a well-established driver of estrogen receptor-positive breast cancer endocrine resistance, promotes estrogen receptor-positive breast cancer brain metastatic colonization in young and aged female mice, through both canonical FGF2/FGFR1 signaling and non-canonical NCAM1/FGFR1 interactions. Astrocytic FGF2-mediated paracrine activation of FGFR1 promotes breast cancer brain metastasis in estrogen-treated young mice, but FGF2 levels and signaling decrease in the brain with aging and estrogen-depletion. Neuronal and astrocytic NCAM1, which remain unchanged in young and aged brains, promote adhesion to neurons, migration, and growth of estrogen receptor-positive cells, suggesting that interactions with astrocytes and neurons facilitate early estrogen receptor-positive breast cancer brain metastasis colonization through FGFR1. Importantly, FDA-approved FGFR inhibitors effectively block early colonization but not late-stage brain metastases, suggesting prevention of FGFR1+ brain metastases as a window of opportunity for FGFR1 inhibitors. - Source: PubMed
Publication date: 2026/05/28
Fox Morgan SJaramillo-Gómez Jenny AMarquez-Ortiz R AlejandroAlvarez-Eraso Karen L FContreras-Zárate Maria JPham Trinh CBarela Elaina NKoliavas Stella NKabos PeterSerkova Natalie JSartorius Carol AWellberg Elizabeth ACittelly Diana M - Immunological changes induced by a woman's first pregnancy in controls and in cases of preeclampsia, which is more frequent and often a more severe complication in primigravid women, were investigated. Decidual natural killer (NK) cells are important for placentation and interact with HLA Ib molecules on extravillous trophoblast cells through specific receptors. In a clinical study part, we identified an increase in the CD56brightCD16-ILT2+ NK subpopulation in peripheral blood in multigravid women compared with primigravidae. Higher levels of decidual-like CD56brightCD16- NK cells in primi- versus multigravid women were observed. The cytotoxic CD56dimCD16+ NK cells and CD56+ NK cells were more abundant in primigravid preeclampsia cases. Other discrepancies in NK subpopulations in preeclampsia according to gravidity were identified in comparison to control pregnancies. The frequency of CD56brightCD16+ NK cells were significantly lower in multigravid control women compared with primigravidae; this was not the case for preeclampsia indicating less induction of CD56brightCD16- NK cells in primigravid women, who develop preeclampsia. Studies of the mechanisms that induce decidual-like NK cells were performed with a human trophoblast-derived cell model with the choriocarcinoma cell line JEG-3 expressing HLA-G. We showed that IL-15 and co-culture with immune cells induce decidual-like CD56brightCD16- NK cells expressing the ILT2 receptor. NK cytotoxicity and CD107a+ degranulation were reduced after such priming. The findings support the development of less cytotoxic NK cells at the fetal-maternal interface of importance for "memory" in subsequent pregnancies and in preeclampsia. - Source: PubMed
Andersen Lærke H JKimmerslev Laura APedersen Nanna HeldagerHave Julie SJepsen Anna KChristensen Maria VMøller Hiba IBøge Rikke NørgaardLarsen Tine GNielsen Henriette SvarreLebech MortenPersson GryHviid Thomas Vauvert F - Multiple myeloma (MM) remains incurable, with drug resistance being a key clinical challenge. Impaired natural killer T (NKT) cell function may contribute to MM immune escape, while the significance of the inhibitory receptor CD161 expression on NKT cells is unclear. This study investigated the association between the peripheral blood CD3⁺CD56⁺CD161⁺ NKT cell proportion and response to bortezomib plus dexamethasone therapy in newly diagnosed MM (NDMM) patients. - Source: PubMed
Zhou SutaoXu XueqingCuo JuanSun ChaoHou YaliWang XiaNana DuanWeixun Shi