Yamina A. Berchiche

1 Introduction Endothelial dysfunction, a hallmark of inflammation, is linked to the pathogenesis of vascular diseases and results in barrier disruption, inflammation and apoptosis (Pober and Sessa, 2007). There are currently limited treatment options for improving endothelial dysfunction resulting in high morbidity and mortality (Dombrovskiy et al., 2007; Goldenberg et al., 2011).

Carlos A. Rico Carlos A. Rico Affiliations Laboratory of Chemical Biology and Signal Transduction, The Rockefeller University, 1230 York Avenue, New York, New York 10065, U.S.A.Tri-Institutional PhD Program in Chemical Biology, The Rockefeller University, 1230 York Avenue, New York, New York 10065, U.S.A. Search for articles by this author Yamina A. Berchiche Yamina A.

The G protein–coupled chemokine receptor CCR5 is required for the cellular entry of HIV-1. The ideal drug targeting CCR5 to block HIV-1 infection would induce receptor internalization without triggering the undesirable effect of inflammation. Thus, Lorenzen et al. characterized the signaling properties of two endogenous ligands of CCR5, RANTES and MIP-1α, and several RANTES analogs in cells expressing CCR5 with G i/o or G q/11 subunits.