CCR2 (human) full length protein-MNP

Plasma membrane-coated nanoparticles (MNPs) have been used in various applications, including delivery of therapeutic agents and induction of immune responses et al. Unlike the conventional strategies, MNPs directly leverage intact and natural functions of cell membranes, and show high biocompatibility, specificity, and low side effects. DIMA biotech developed an optimized MNPs platform for the full-length membrane protein productions using membrane coating technology and HEK293 based expression platform. The high-purity plasma membrane-coated nanoparticles were produced by extrusion after membrane extraction from the host HEK293 cells containing the overexpressed target proteins. Protein function: Key functional receptor for CCL2 but can also bind CCL7 and CCL12 (PubMed:8146186, PubMed:8048929, PubMed:23408426). 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 (Probable). 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]