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Updated: May 31, 2026

Tracking Drug-induced Changes in Receptor Post-internalization Trafficking by Colocalizational Analysis
Published on: July 3, 2015
Prostacyclin receptor regulation--from transcription to trafficking
C Midgett1, J Stitham, K A Martin
1Department of Internal Medicine, Section of Cardiovascular Medicine, Yale School of Medicine, Cardiovascular Research Center, 300 George Street, Rm 759H, New Haven, CT 06511, USA.
Abstract:
The prostacyclin receptor (IP--International Union of Pharmacology nomenclature) is a member of the seven transmembrane G-protein coupled receptor (GPCR) superfamily. Recent concerns with selective and non-selective COX-1/COX-2 inhibition have exposed an important cardioprotective role for IP in preventing atherothrombosis. Receptor dysfunction (genetic variants) or reduced signaling (COX-2 inhibition) in high cardiovascular risk patients leads to increased cardiovascular events. These clinical observations have also been confirmed genetically by mouse knockout studies. Thus, receptor regulation is paramount in ensuring correct function in the prevention of atherothrombosis. This review summarizes recent literature on how this important receptor is regulated, from transcription to transport (to and from the membrane surface). These regulatory processes are critical in ensuring that IP receptors are adequately expressed and functional on the cell surface.
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