Structure and Regulation of G Protein-Coupled Receptors: The β2-Adrenergic Receptor as a Model

1991 ◽  
pp. 1-39 ◽  
Author(s):  
Sheila Collins ◽  
Martin J. Lohse ◽  
Brian O'Dowd ◽  
Marc G. Caron ◽  
Robert J. Lefkowitz
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
G Protein Coupled Receptors ◽  
Β2 Adrenergic Receptor ◽  
G Protein Coupled

Rab1 interacts directly with the β2-adrenergic receptor to regulate receptor anterograde trafficking

2012 ◽  
Vol 393 (6) ◽  
pp. 541-546 ◽  
Author(s):  
Maha M. Hammad ◽  
Yi-Qun Kuang ◽  
Alexa Morse ◽  
Denis J. Dupré
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
G Protein ◽  
Adrenergic Receptor ◽  
Direct Interaction ◽  
Potential Interaction ◽  
G Protein Coupled Receptors ◽  
Endocytic Pathway ◽  
Β2 Adrenergic Receptor ◽  
G Protein Coupled

Abstract Very little is understood about the trafficking of G protein-coupled receptors (GPCRs) from the endoplasmic reticulum (ER) to the plasma membrane. Rab guanosine triphosphatases (GTPases) are known to participate in the trafficking of various GPCRs via a direct interaction during the endocytic pathway, but whether this occurs in the anterograde pathway is unknown. We evaluated the potential interaction of Rab1, a GTPase known to regulate β2-adrenergic receptor (β2AR) trafficking, and its effect on export from the ER. Our results show that GTP-bound Rab1 interacts with the F(x)6LL motif of β2AR. Receptors lacking the interaction motif fail to traffic properly, suggesting that a direct interaction with Rab1 is required for β2AR anterograde trafficking.

Members of the G Protein-Coupled Receptor Kinase Family That Phosphorylate the β2-Adrenergic Receptor Facilitate Sequestration†

Biochemistry ◽  
1996 ◽  
Vol 35 (13) ◽  
pp. 4155-4160 ◽  
Author(s):  
Luc Ménard ◽  
Stephen S. G. Ferguson ◽  
Larry S. Barak ◽  
Lucie Bertrand ◽  
Richard T. Premont ◽  
...  
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Kinase Family ◽  
Β2 Adrenergic Receptor ◽  
G Protein Coupled

G-protein coupled receptor auto-antibodies in thromboangiitis obliterans (Buerger’s disease) and their removal by immunoadsorption

VASA ◽  
2014 ◽  
Vol 43 (5) ◽  
pp. 347-352 ◽  
Author(s):  
Peter F. Klein-Weigel ◽  
Marion Bimmler ◽  
Petra Hempel ◽  
Sebastian Schöpp ◽  
Siegrid Dreusicke ◽  
...  
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
G Protein Coupled Receptors ◽  
Thromboangiitis Obliterans ◽  
Therapeutic Effects ◽  
Study Group ◽  
Eta Receptor ◽  
Serological Data ◽  
Agonistic Autoantibodies ◽  
G Protein Coupled

Background: Immunhistopathological and serological data favors an immunopathogenesis of thromboangiitis onliterans(TAO, Buerger’s disease). Autoantbodies seem to play a major role. Immunoadsorption (IA) proved to be therapeutically effective. We focused on agonistic autoantibodies (agAAB) directed against G-protein coupled receptors (GPCR) and proved the hypothesis, that these agAAB might be present in TAO and that a five day course of IA might be able to eliminate these agAAB effectively. Patients and methods: Between December 2012 and May 2014 11 TAO-patients were treated by IA in a five day course. AgAAB-analysis was performed using specific ELISA techniques. Results: AgAAB were detected in 9 out of 11 patients (81.8 %).Multiple agAAB were present in 7 patients (63.6 %). A clustering of agAAB directed against loop1 of the adrenergic α1-receptor and the endothelin-A-(ETA)receptor was identified, representing 72.7 % resp. 54.5 % of the patients. AgAAB directed against the angiotensin-1 (AT-1) epitope 1 or 2 were detected in 3 patients and agAAB directed against protease-activated receptor (PAR) loop1/2 were seen in 2 patients. AgAAB directed against ETA-receptor loop1 never appeared without agAAB directed against α1-receptor loop1. Immediately after a five day-course of IA agAAB were absent in 81.8 % of the total study group and in 77.8 % of all cases tested positive for agAAB before IA. Conclusions: AgAAB directed against GPCR were identified in TAO patients with a clustering of agAAB directed against α-1-adrenergic receptor loop1 and ETA-receptor loop1. AgAA were eliminated by IA in the majority of cases. We suggest that these agAA play an important role in the pathogenesis of TAO and that their elimination might be responsible for the positive therapeutic effects reported in patients treated with IA.

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