scholarly journals Two peptides from the alpha 2A-adrenergic receptor alter receptor G protein coupling by distinct mechanisms

1991 ◽  
Vol 266 (17) ◽  
pp. 11025-11029 ◽  
Author(s):  
H.M. Dalman ◽  
R.R. Neubig
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
G Protein Coupling ◽  
Protein Coupling

Halothane disruption of α2-adrenergic receptor-mediated inhibition of adenylate cyclase and receptor G-protein coupling in rat brain

1990 ◽  
Vol 39 (1) ◽  
pp. 223-225 ◽  
Author(s):  
Melissa K. Baumgartner ◽  
Robert L. Dennison ◽  
Tanjore K. Narayanan ◽  
Robert S. Aronstam
Keyword(s):  
Adenylate Cyclase ◽  
Rat Brain ◽  
G Protein ◽  
Adrenergic Receptor ◽  
G Protein Coupling ◽  
Protein Coupling

scholarly journals A Gain-of-function Polymorphism in a G-protein Coupling Domain of the Human β1-Adrenergic Receptor

1999 ◽  
Vol 274 (18) ◽  
pp. 12670-12674 ◽  
Author(s):  
Deborah A. Mason ◽  
J. Donald Moore ◽  
Stuart A. Green ◽  
Stephen B. Liggett
Keyword(s):  
G Protein ◽  
Adrenergic Receptor ◽  
Gain Of Function ◽  
G Protein Coupling ◽  
Protein Coupling

Spinal nerve ligation increases α2-adrenergic receptor G-protein coupling in the spinal cord

2005 ◽  
Vol 1038 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Carsten Bantel ◽  
James C. Eisenach ◽  
Frederic Duflo ◽  
Joseph R. Tobin ◽  
Steven R. Childers
Keyword(s):  
Spinal Cord ◽  
G Protein ◽  
Adrenergic Receptor ◽  
Spinal Nerve ◽  
Spinal Nerve Ligation ◽  
G Protein Coupling ◽  
Protein Coupling

scholarly journals The IgG3 subclass of β1-adrenergic receptor autoantibodies is an endogenous biaser of β1AR signaling

2021 ◽  
Vol 32 (7) ◽  
pp. 622-633
Author(s):  
Maradumane L. Mohan ◽  
Yuji Nagatomo ◽  
Prasenjit Prasad Saha ◽  
Sromona D. Mukherjee ◽  
Timothy Engelman ◽  
...  
Keyword(s):  
Heart Failure ◽  
G Protein ◽  
Adrenergic Receptor ◽  
Human Heart ◽  
Human Heart Failure ◽  
G Protein Coupling ◽  
Protein Coupling ◽  
Igg3 Subclass

β1-Adrenergic receptor autoantibodies are associated with deleterious consequences; however, the IgG3 subclass provides beneficial outcomes in human heart failure. IgG3 β1AR autoantibody inhibits G-protein coupling, simultaneously activating ERK through G-protein–independent arrestin-dependent mechanisms.

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