Purified Anti-Human CD192 Antibody[K036C2]

CCR2 is a chemokine receptor that binds monocyte chemoattractant proteins (MCP-1, 2, 3 and 4). Two spliced variants were initially described for CCR2 (CCR2A and CCR2B). These variants differ in their terminal carboxyl tails. Monocyte adhesion to the arterial endothelium and subsequent migration into the intima are central events in the pathogenesis of atherosclerosis. CCR2 and MCP-1 have been associated to atherosclerotic plaques. MCP-1 is induced by modified-LDL in endothelial cells and may trigger firm adhesion of monocytes to vascular endothelium under flow conditions. Local overexpression of MCP-1 at vessel walls induces infiltration of macrophages and formation of atherosclerotic lesions. Obesity induces an inflammatory state that is implicated in many clinically important complications, including insulin resistance, diabetes, atherosclerosis, and non-alcoholic fatty liver disease. CCR2 influences the development of obesity and associated adipose tissue inflammation. Protein function: Key functional receptor for CCL2 but can also bind CCL7, and CCL12 (PubMed:23408426, PubMed:38157855, PubMed:8048929, PubMed:8146186). Also transduces signaling mediated by CCL13 (PubMed:38157855). Its binding with CCL2 on monocytes and macrophages mediates chemotaxis and migration induction through the activation of the PI3K cascade, the small G protein Rac and lamellipodium protrusion (PubMed:38157855). Also acts as a receptor for the beta-defensin DEFB106A/DEFB106B (PubMed:23938203). Regulates the expression of T-cell inflammatory cytokines and T-cell differentiation, promoting the differentiation of T-cells into T-helper 17 cells (Th17) during inflammation. Facilitates the export of mature thymocytes by enhancing directional movement of thymocytes to sphingosine-1-phosphate stimulation and up-regulation of S1P1R expression, signals through the JAK-STAT pathway to regulate FOXO1 activity leading to an increased expression of S1P1R. Plays an important role in mediating peripheral nerve injury-induced neuropathic pain. Increases NMDA-mediated synaptic transmission in both dopamine D1 and D2 receptor-containing neurons, which may be caused by MAPK/ERK-dependent phosphorylation of GRIN2B/NMDAR2B. Mediates the recruitment of macrophages and monocytes to the injury site following brain injury. [The UniProt Consortium]