CD204 Monoclonal Antibody (PSL204), PE-Cyanine7, eBioscience™, Invitrogen™

Description

• This monoclonal antibody PSL204 reacts with human CD204, also known as Macrophage Scavenger Receptor 1 (MSR1), Scavenger Receptor Type A (SR-A), or SCARA1
• It is expressed by multiple populations of macrophages and dendritic cells
• CD204 belongs to the class A family of scavenger receptors, a group of five homotrimetric transmembrane proteins that contain a short cytoplasmic tail and extracellular C -terminus
• Other members of this family include: MARCO (SCARA2), CSR (SCARA3), SRCL (SCARA4) and SCARA5
• CD204 binds and internalizes oxidized low density lipoproteins (LDL), which drives macrophage differentiation into foam cells, secretion of inflammatory cytokines, and development of atherosclerotic lesions
• In addition to oxidized LDL, CD204 binds and uptakes a wide variety of macromolecules, including bacterial cell wall components, viral DNA, calciprotein complexes, apoptotic cells, and beta-amyloid fibrils
• This broad binding specificity implicates CD204-expressing macrophages in a number of physiological processes and pathologies, such as host defense, inflammation, bone remodeling, atherosclerosis, sepsis, and Alzheimer's disease
• In humans, CD204 exists as 3 splice variants
• The more ubiquitous full length isoform (type I, SR-AI), a shorter isoform (type II, SR-AII) that lacks the C-terminal cysteine-rich domain, and the shortest isoform (type III, SR-AIII)
• CD204 gene encodes the class A macrophage scavenger receptors, which include three different types (1, 2, 3) generated by alternative splicing of this gene
• These receptors or isoforms are macrophage-specific trimeric integral membrane glycoproteins and have been implicated in many macrophage-associated physiological and pathological processes including atherosclerosis, Alzheimer's disease, and host defense
• The isoforms type 1 and type 2 are functional receptors and are able to mediate the endocytosis of modified low density lipoproteins (LDLs)
• The isoform type 3 does not internalize modified LDL (acetyl-LDL) despite having the domain shown to mediate this function in the types 1 and 2 isoforms
• It has an altered intracellular processing and is trapped within the endoplasmic reticulum, making it unable to perform endocytosis
• The isoform type 3 can inhibit the function of isoforms type 1 and type 2 when co-expressed, indicating a dominant negative effect and suggesting a mechanism for regulation of scavenger receptor activity in macrophages
• Diseases associated with MSR1 include Barrett Esophagus and Prostate Cancer.