Anti-Recombinant LY9/CD229/SLAMF3, clone 8A6

Signaling lymphocytic activation molecule 3 (SLAMF3), also known as CD229 or Ly9, is a type I transmembrane glycoprotein that belongs to the SLAM family receptors (PMID: 10970093, 15905546). It is composed of an extracellular region, which consists of four Ig-like domains, a transmembrane region, and a cytoplasmic tail, which includes two immunoreceptor tyrosine-based signaling motifs (ITSMs) and other tyrosine residues that act as binding sites for the SH2 structural domains (PMID: 8537117, 11369645, 38626547). SLAMF3 is mainly expressed in immune cells, such as T, B, and natural killer cells, and it is involved in the fundamental activation and suppression of these immune cells, as well as the regulation of complex immune networks (PMID: 38626547). Protein function: Self-ligand receptor of the signaling lymphocytic activation molecule (SLAM) family. SLAM receptors triggered by homo- or heterotypic cell-cell interactions are modulating the activation and differentiation of a wide variety of immune cells and thus are involved in the regulation and interconnection of both innate and adaptive immune response. Activities are controlled by presence or absence of small cytoplasmic adapter proteins, SH2D1A/SAP and/or SH2D1B/EAT-2 (PubMed:19648922). May participate in adhesion reactions between T lymphocytes and accessory cells by homophilic interaction. Promotes T- cell differentiation into a helper T-cell Th17 phenotype leading to increased IL-17 secretion, the costimulatory activity requires SH2D1A. Promotes recruitment of RORC to the IL-17 promoter. May be involved in the maintenance of peripheral cell tolerance by serving as a negative regulator of the immune response. May disable autoantibody responses and inhibit IFN-gamma secretion by CD4(+) T- cells (PubMed:23914190). May negatively regulate the size of thymic innate CD8(+) T-cells and the development of invariant natural killer T (iNKT) cells (PubMed:23225888). Can promote natural killer (NK) cell activation (PubMed:19648922). [The UniProt Consortium]