{Reference Type}: Journal Article
{Title}: Hijacking of GPCRs and RTKs by pathogens.
{Author}: Ayoub MA;
{Journal}: Cell Signal
{Volume}: 109
{Issue}: 0
{Year}: 2023 Sep 10
{Factor}: 4.85
{DOI}: 10.1016/j.cellsig.2023.110802
{Abstract}: Pathogens exploit multiple cellular and molecular pathways in the host organisms for their entry, survival and dissemination. The cell surface receptors such as G protein-coupled receptors (GPCRs) and receptor tyrosine kinases (RTKs) constitute the targets of many pathogens. This is due to the ubiquitous expression of these two receptor families in the organism and their pivotal role in various cellular and physiological processes. At the molecular level, receptor hijacking implies either direct or indirect interactions between pathogens' effectors or toxins with GPCRs and RTKs at the cell surface thereby interfering with their activation and their downstream signaling pathways inside the host cells. As a result, the pathogens manipulate and redirect GPCR/RTK-mediated signaling pathways and different aspects of cell function for their benefit. The review presents a compilation of the major examples of pathogen infections where GPCRs and RTKs and their related intracellular signaling pathways are targeted. This provides a molecular basis for pathogens hijacking cell signaling and their virulence. Our understanding of such complex host-pathogen interactions at the molecular level will open new opportunities to develop new prophylactic and therapeutic approaches against infections. In this context, the pharmacological targeting of GPCRs and RTKs may be a promising approach.