Clathrin‐Dependent Mechanisms of G Protein‐coupled Receptor Endocytosis

The heptahelical G protein‐coupled receptor (GPCR) family includes ∼900 members and is the largest family of signaling receptors encoded in the mammalian genome. G protein‐coupled receptors elicit cellular responses to diverse extracellular stimuli at the plasma membrane and some internalized recept...

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Bibliographic Details
Published in:Traffic (Copenhagen, Denmark) Denmark), 2007-05, Vol.8 (5), p.462-470
Main Authors: Wolfe, Breann L., Trejo, JoAnn
Format: Article
Language:English
Subjects:
actin
Actins - physiology
Adaptor Proteins, Vesicular Transport - physiology
AP2
arrestin
Arrestins - physiology
Clathrin - physiology
dynamin
Endocytosis - physiology
epsin
GPCR
internalization
Models, Biological
numb
Receptors, G-Protein-Coupled - metabolism
trafficking
ubiquitin
Ubiquitin - metabolism
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Summary:The heptahelical G protein‐coupled receptor (GPCR) family includes ∼900 members and is the largest family of signaling receptors encoded in the mammalian genome. G protein‐coupled receptors elicit cellular responses to diverse extracellular stimuli at the plasma membrane and some internalized receptors continue to signal from intracellular compartments. In addition to rapid desensitization, receptor trafficking is critical for regulation of the temporal and spatial aspects of GPCR signaling. Indeed, GPCR internalization functions to control signal termination and propagation as well as receptor resensitization. Our knowledge of the mechanisms that regulate mammalian GPCR endocytosis is based predominantly on arrestin regulation of receptors through a clathrin‐ and dynamin‐dependent pathway. However, multiple clathrin adaptors, which recognize distinct endocytic signals, are now known to function in clathrin‐mediated endocytosis of diverse cargo. Given the vast number and diversity of GPCRs, the complexity of clathrin‐mediated endocytosis and the discovery of multiple clathrin adaptors, a single universal mechanism controlling endocytosis of all mammalian GPCRs is unlikely. Indeed, several recent studies now suggest that endocytosis of different GPCRs is regulated by distinct mechanisms and clathrin adaptors. In this review, we discuss the diverse mechanisms that regulate clathrin‐dependent GPCR endocytosis.
ISSN:1398-9219
1600-0854
DOI:10.1111/j.1600-0854.2007.00551.x