CCR2b Protein-VLP, Human (HEK293)

The CCR2b Protein-VLP serves as a crucial functional receptor for CCL2 and can also bind to CCL7 and CCL12. Its interaction with CCL2 on monocytes and macrophages facilitates chemotaxis and induces migration by activating the PI3K cascade, small G protein Rac, and lamellipodium protrusion. Additionally, it acts as a receptor for the beta-defensin DEFB106A/DEFB106B and regulates the expression of T-cell inflammatory cytokines, promoting the differentiation of T-cells into T-helper 17 cells (Th17) during inflammation. CCR2b facilitates the export of mature thymocytes by enhancing directional movement in response to sphingosine-1-phosphate stimulation and up-regulating S1P1R expression through JAK-STAT signaling. It plays a crucial role in mediating neuropathic pain induced by peripheral nerve injury and increases NMDA-mediated synaptic transmission in dopamine D1 and D2 receptor-containing neurons. Furthermore, CCR2b is involved in the recruitment of macrophages and monocytes to the injury site following brain injury. In the context of microbial infection, it serves as an alternative coreceptor with CD4 for HIV-1 infection.