CCR2 (human) full length protein-synthetic nanodisc

Discover a breakthrough in membrane protein research and drug development with DIMA Biotech's Synthetic Nanodiscs. Traditional methods struggle with challenges in obtaining water-soluble and bioactive forms of multi-transmembrane proteins. Our innovative polymer-based Nanodisc platform offers a game-changing solution by excluding membrane scaffold proteins (MSPs), resulting in a cleaner system with fewer interferences for downstream assays. By disassembling cell membranes into nanoscale disc-shaped structures, our technology enables the purification of membrane proteins to high homogeneity under aqueous conditions. Explore how Synthetic Nanodiscs empower the functional characterization of multi-span transmembrane proteins in their active form, revolutionizing the future of membrane protein research and drug development. 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]