CD150 antibody
- Known as:
- CD150 (anti-)
- Catalog number:
- orb101809
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CD150 antibody
Related genes to: CD150 antibody
- Gene:
- SLAMF1 NIH gene
- Name:
- signaling lymphocytic activation molecule family member 1
- Previous symbol:
- SLAM
- Synonyms:
- CD150
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-06
- Date modifiied:
- 2014-11-18
Related products to: CD150 antibody
Related articles to: CD150 antibody
- - Source: PubMed
Publication date: 2026/06/09
Forman Oliver PFreyer JamieKerr AbigailLabadie Julia DGow Debbie JAlexander Janet - Innate lymphocytes and myeloid cells communicate and play an essential part in activating neutrophils and other effector cells to kill fungi. Here, we identified that Signaling Lymphocytic Activation Molecule 1 (SLAMF1) orchestrates a cellular and molecular signaling network that activates phagocytes. We uncovered innate lymphocytes including innate CD4+ or TCRγδ+ T cells augment neutrophil killing of Blastomyces dermatitidis (Bd) in a SLAMF1 dependent manner. SLAMF1 expression on neutrophils enabled homotypic SLAMF1:SLAMF1 interactions with innate CD4+ T cells, which released soluble factors that activated neutrophils to kill fungi. Our work furnishes new mechanistic insight about the role of SLAMF1 in mobilizing innate immune cells to induce phagocyte-driven killing of inhaled fungi. - Source: PubMed
Publication date: 2026/05/28
Lau Lindsay SuarezLichtenberger SarahTaira Cleison LedesmaKlein Bruce SWüthrich Marcel - Measles virus (MeV) infection is mediated by two cellular receptors: signaling lymphocytic activation molecule family member 1 (SLAMF1, also known as CD150), expressed by immune cells, and nectin-4, expressed by epithelial cells. Infection of immune cells causes systemic disease and immune suppression, while infection of airway epithelial cells results in efficient transmission. In rare cases, MeV reaches the brain and slowly spreads in cells that do not express bona fide receptors, causing subacute sclerosing panencephalitis (SSPE). In the brains of persons with SSPE, multiple mutations of the MeV membrane fusion apparatus are selected that enable its triggering by host proteins acting as surrogate receptors. These mutations favor cell-to-cell spread, which promotes population-based MeV genome evolution and the formation of collective infectious units (CIUs). CIUs, which can rebalance their components and rapidly adapt to new environments, may support neuropathogenesis of other nonintegrating RNA viruses, in particular those with nonsegmented negative-strand genomes. - Source: PubMed
Publication date: 2026/04/28
Cattaneo RobertoYadav Kalpanade Vries Rory Dde Swart Rik L - Signaling lymphocytic activation molecule family member 1 (SLAMF1/CD150) is a multifunctional receptor that regulates both innate and adaptive immunity. Through homophilic interactions and SAP-dependent signaling, SLAMF1 supports invariant natural killer T (iNKT) cell selection, γδ T cell polarization, and natural killer (NK) cell education. It also modulates germinal center dynamics and humoral responses, often in cooperation with other SLAM receptors. Beyond lymphoid compartments, SLAMF1 functions as a microbial sensor in macrophages, promotes phagosome maturation, reactive oxygen species production, and regulates Toll-like receptor 4 (TLR4)-mediated pathways, thereby linking innate recognition to antimicrobial defense. Dysregulation of SLAMF1 has been implicated in diverse pathological conditions. In chronic lymphocytic leukemia, its loss associates with genomic instability, poor outcomes, and therapy resistance, while in trophoblastic tumors and renal cell carcinoma, elevated expression sustains tumor survival and progression. In autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, SLAMF1 drives pathogenic T-B collaboration and chronic inflammation. Infectious disease studies further highlight its role as both a pathogen sensor and viral entry receptor. Recent therapeutic advances, including SLAMF1-derived peptides, offer innovative strategies for modulating inflammation, protecting against cardiac injury, and selectively inducing tumor cell apoptosis. These findings establish SLAMF1 as a biomarker and promising therapeutic target, warranting further translational investigation. - Source: PubMed
Publication date: 2026/03/21
Ahmad IrfanAltalbawy Farag M ABishoyi Ashok KumarBallal SuhasSingh AbhayveerDevi AnitaSharma Girish ChandraAminov ZafarBhakuni Pushpa NegiZwamel Ahmed Hussein - Neutrophils and monocytes are the main fungal effector cells in restricting ( and other fungi at the respiratory mucosa. However, understanding how phagocytes become activated and recruited to the site of infection is still incompletely understood. Innate lymphocytes and myeloid cells have been found to communicate and play an essential part in activating neutrophils and other effector cells to kill fungi. Here, we identified that Signaling Lymphocytic Activation Molecule 1 (SLAMF1) is a key host immune receptor involved in orchestrating a cellular and molecular signaling network that leads to the activation of phagocytes. By using mice to conditionally eliminate SLAMF1 receptor expression on innate CD4 or TCRγδ T cells, we uncovered that these innate lymphocytes augment neutrophil killing of in a SLAMF1 dependent manner. SLAMF1 expression on neutrophils enabled homotypic SLAMF1:SLAMF1 interactions with innate CD4 T cells, which prompted release of soluble factors that activated neutrophils to kill fungi. Our work furnishes new mechanistic insight about the role of SLAMF1 in mobilizing innate immune cells to induce phagocyte-driven killing of inhaled fungi. - Source: PubMed
Publication date: 2026/02/20
Lau Lindsay SLichtenberger SarahTaira Cleison LedesmaKlein Bruce SWüthrich Marcel