Abstract
G-protein–coupled receptors (GPCRs) are targets for around one third of currently approved and clinical prescribed drugs and represent the largest and most structurally diverse family of transmembrane signaling proteins, with almost 1000 members identified in the human genome. Upon agonist stimulation, GPCRs are internalized and trafficked inside the cell: they may be targeted to different organelles, recycled back to the plasma membrane or be degraded. Once inside the cell, the receptors may initiate other signaling pathways leading to different biological responses. GPCRs’ biological function may also be influenced by interaction with other receptors. Thus, the ultimate cellular response may depend not only on the activation of the receptor from the cell membrane, but also from receptor trafficking and/or the interaction with other receptors. This review is focused on angiotensin receptors and how their biological function is influenced by trafficking and interaction with others receptors.
Highlights
The renin-angiotensin system (RAS) exerts a fundamental role in blood pressure control and fluid homeostasis
In transfected HeLa cells, angiotensin II (Ang II) type 2 receptor (AT2R) inhibits the signaling of Ang II type 1 receptor (AT1R) that is induced by the ligand through a pathway dependent on protein kinase C (PKC) activation, and this effect results from constitutive AT1RAT2R heteromerization (Inuzuka et al, 2016)
Sustained binding of AT1R to b-arrestin induces trafficking to late endosomes and lysosomes, promoting receptor down-regulation and terminating intracellular signaling pathways activated by Ang II/AT1R (Dale et al, 2004; Toth et al, 2018b)
Summary
The renin-angiotensin system (RAS) exerts a fundamental role in blood pressure control and fluid homeostasis. In transfected HeLa cells, AT2R inhibits the signaling of AT1R that is induced by the ligand through a pathway dependent on protein kinase C (PKC) activation, and this effect results from constitutive AT1RAT2R heteromerization (Inuzuka et al, 2016).
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
