Sialic acid mediated mechanical activation of β₂ adrenergic receptors by bacterial pili.

ABSTRACT: Meningococcus utilizes β-arrestin selective activation of endothelial cell β₂ adrenergic receptor (β₂AR) to cause meningitis in humans. Molecular mechanisms of receptor activation by the pathogen and of its species selectivity remained elusive. We report that β₂AR activation requires two asparagine-branched glycan chains with terminally exposed N-acetyl-neuraminic acid (sialic acid, Neu5Ac) residues located at a specific distance in its N-terminus, while being independent of surrounding amino-acid residues. Meningococcus triggers receptor signaling by exerting direct and hemodynamic-promoted traction forces on β₂AR glycans. Similar activation is recapitulated with beads coated with Neu5Ac-binding lectins, submitted to mechanical stimulation. This

SUBMITTER: Virion Z 

PROVIDER: S-EPMC6800425 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature