Unrestrained Gα_i2 Signaling Disrupts Neutrophil Trafficking, Aging, and Clearance.

ABSTRACT: Neutrophil trafficking, homeostatic and pathogen elicited, depends upon chemoattractant receptors triggering heterotrimeric G-protein Gα_iβγ signaling, whose magnitude and kinetics are governed by RGS protein/Gα_i interactions. RGS proteins typically limit Gα_i signaling by reducing the duration that Gα_i subunits remain GTP bound and able to activate downstream effectors. Yet how in totality RGS proteins shape neutrophil chemoattractant receptor activated responses remains unclear. Here, we show that C57Bl/6 mouse neutrophils containing a genomic knock-in of a mutation that disables all RGS protein-Gα_i2 interactions (G184S) cannot properly balance chemoattractant receptor signaling, nor appropriately respond to inflammatory insults

SUBMITTER: Yan SL 

PROVIDER: S-EPMC8202015 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature