bioRxiv Science⌕ Search

Biology subjects

Grahl, A.

Publications and source records attributed to Grahl, A..

2 recordsLinked to original sources

Filling of a water-free void explains the allosteric regulation of the β1-adrenergic receptor by cholesterol

Proteins often contain cavities, which are usually assumed to be water-filled. Recent high-pressure NMR results indicate that the preactive conformation of the {beta}1-adrenergic receptor ({beta}1AR) contains completely empty cavities (dry voids) of about [~]100 [A]3 volume, which disappear in the active conformation of the receptor. Here we have localized these cavities by X-ray crystallography on xenon-derivatized {beta}1AR crystals. One of the cavities coincides with the binding pocket of cholesterol. Solution NMR data show that addition of the soluble cholesterol analog cholesteryl hemisuccinate (CHS) impedes the formation of the active conformation of the receptor by blocking conserved GPCR microswitches. This wedge-like action explains the function of the cellularly highly abundant cholesterol as a negative allosteric modulator of {beta}1AR. The detailed understanding of GPCR regulation by cholesterol via filling of a dry void and the easy scouting for such voids by xenon may provide new routes for the development of allosteric drugs.

biophysics↗

Structural basis of the activation of the CC chemokine receptor 5 by a chemokine agonist

The human CC chemokine receptor 5 (CCR5) is a G protein-coupled receptor (GPCR) that plays a major role in inflammation and is involved in the pathology of cancer, HIV, and COVID-19. Despite its significance as a drug target, the activation mechanism of CCR5, i.e. how chemokine agonists transduce the activation signal through the receptor, is yet unknown. Here, we report the cryo-EM structure of wild-type CCR5 in an active conformation bound to the chemokine super-agonist [6P4]CCL5 and the heterotrimeric Gi protein. The structure provides the rationale for the sequence-activity relation of agonist and antagonist chemokines. The N-terminus of agonist chemokines pushes onto an aromatic connector that transmits activation to the canonical GPCR microswitch network. This activation mechanism differs significantly from other CC chemokine receptors that bind shorter chemokines in a shallow binding mode and have unique sequence signatures and a specialized activation mechanism. One-sentence summaryThe structure of CCR5 in complex with the chemokine agonist [6P4]CCL5 and the heterotrimeric Gi protein reveals its activation mechanism

biophysics↗