FIGURE 1.

CCR5 receptor signaling pathways. When the amino terminus of CCR5 binds to its ligand, its following signaling pathway is mainly controlled by Gα_q, Gα_i, and βγ subunits. The Gα_i pathway results in the release of intracellular Ca²⁺ and decreased learning and memory function, as well as worsened recovery from neuronal damage by reduced cAMP and pCREB. Activation of Gα_q results in cell migration and cytokine expression in immune response. And the βγ subunits leads to cell survival, adhesion and motility through multiple following signaling pathways such as AKT/PKB and Rho GTPase. AC, adenylyl cyclase; AD, Alzheimer’s disease; AKT/PKB, protein kinase B; cAMP, cyclic adenosine monophosphate; CCR5, C–C chemokine receptor 5; CREB, cAMP-response-element binding protein; DAG, diacylglycerol; HAND, HIV-related neurocognitive disorders; IP3, inositol 1,4,5-trisphosphate; JNK, C-Jun N-terminal kinases; MS, multiple sclerosis; pCREB, phosphorylated cAMP-response-element binding protein; PKB/Akt, protein kinase B; PKC, protein kinase C; PLC, phospholipase C.