General Notes
Mouse anti Human Sphingosine 1-Phosphate Receptor 1, clone 2B9 recognizes S1P1, otherwise known as CD363/EDG-1, a bioactive lysophospholipid and inducible member of the G-protein coupled receptor superfamily (GPCR) which plays an important role in a variety of cellular processes. During inflammatory diseases such as atherosclerosis the phenotype switching of activated macrophages is influenced by the presence of particular cytokines within the microenvironment. These cells have been characterized as classically activated M1 macrophages, in response to pro-inflammatory molecules such as interferon gamma and lipopolysaccharide, or as alternatively activated M2 macrophages, in response to anti-inflammatory cytokines such as interleukin-4. Activation of S1P1 through its ligand S1P (Sphingosine 1-Phosphate) has been identified as an important promoter of anti-inflammatory M2 macrophages (Hughes et al. 2008). Apoptotic cells can also influence the pro-versus anti-inflammatory macrophage response, and S1P acts as a positive regulator for anti-apoptotic/pro-survival responses by binding to S1P1. Growing evidence suggests that the expression of S1P1 on macrophages may convey protection against apoptosis, at least in part, having implications for the pathogenesis of inflammatory diseases and cancer. Deviation in sphingosine 1-phosphate (S1P) signaling is important in many types of cancer. Analysis of S1P1 and SK1 receptors during the development of tamoxifen resistance in Estrogen Receptor (ER) breast cancer patients concurs that the expression levels of S1P1 correlates with tumor size and Progesterone Receptor (PR) status and that high S1P1 membrane expression is associated with shorter time to recurrence.