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GPCRs and Arrestins in Airways: Implications for Asthma.
MedLine Citation:
PMID:  24292841     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
The obstructive lung disease asthma is treated by drugs that target, either directly or indirectly, G protein-coupled receptors (GPCRs). GPCRs coupled to Gq are the primary mediators of airway smooth muscle (ASM) contraction and increased airway resistance, whereas the Gs-coupled beta-2-adrenoceptor (β2AR) promotes pro-relaxant signaling in and relaxation of ASM resulting in greater airway patency and reversal of life-threatening bronchoconstriction. In addition, GPCR-mediated functions in other cell types, including airway epithelium and hematopoietic cells, are involved in the control of lung inflammation that causes most asthma. The capacity of arrestins to regulate GPCR signaling, via either control of GPCR desensitization/resensitization or G protein-independent signaling, renders arrestins an intriguing therapeutic target for asthma and other obstructive lung diseases. This review will focus on the potential role of arrestins in those GPCR-mediated airway cell functions that are dysregulated in asthma.
Authors:
Raymond B Penn; Richard A Bond; Julia K L Walker
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Handbook of experimental pharmacology     Volume:  219     ISSN:  0171-2004     ISO Abbreviation:  Handb Exp Pharmacol     Publication Date:  2014  
Date Detail:
Created Date:  2013-12-02     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7902231     Medline TA:  Handb Exp Pharmacol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  387-403     Citation Subset:  IM    
Affiliation:
Center for Translational Medicine, Department of Medicine, Jefferson Medical College, Thomas Jefferson University, 1025 Walnut Street, Suite 317, Philadelphia, PA, 19107, USA, Raymond.Penn@jefferson.edu.
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