scholarly journals G-protein-coupled receptor inactivation by an allosteric inverse-agonist antibody

Nature ◽  
2012 ◽  
Vol 482 (7384) ◽  
pp. 237-240 ◽  
Author(s):  
Tomoya Hino ◽  
Takatoshi Arakawa ◽  
Hiroko Iwanari ◽  
Takami Yurugi-Kobayashi ◽  
Chiyo Ikeda-Suno ◽  
...  
Keyword(s):  
G Protein ◽  
Inverse Agonist ◽  
G Protein Coupled Receptor ◽  
Receptor Inactivation ◽  
Agonist Antibody ◽  
G Protein Coupled

scholarly journals The extracellular N-terminal domain of G-protein coupled receptor 83 regulates signaling properties and is an intramolecular inverse agonist

2014 ◽  
Vol 7 (1) ◽  
pp. 913 ◽  
Author(s):  
Anne Müller ◽  
Brinja Leinweber ◽  
Jana Fischer ◽  
Timo D Müller ◽  
Annette Grüters ◽  
...  
Keyword(s):  
G Protein ◽  
Inverse Agonist ◽  
G Protein Coupled Receptor ◽  
Terminal Domain ◽  
G Protein Coupled

scholarly journals Identification of the First Nonpeptidergic Inverse Agonist for a Constitutively Active Viral-encoded G Protein-coupled Receptor

2002 ◽  
Vol 278 (7) ◽  
pp. 5172-5178 ◽  
Author(s):  
Paola Casarosa ◽  
Wiro M. Menge ◽  
Rosalba Minisini ◽  
Claas Otto ◽  
Jane van Heteren ◽  
...  
Keyword(s):  
G Protein ◽  
Inverse Agonist ◽  
G Protein Coupled Receptor ◽  
G Protein Coupled ◽  
Constitutively Active

scholarly journals Nitric Oxide and S-Nitrosylation in Cardiac Regulation: G Protein-Coupled Receptor Kinase-2 and β-Arrestins as Targets

2021 ◽  
Vol 22 (2) ◽  
pp. 521
Author(s):  
Gizem Kayki-Mutlu ◽  
Walter J. Koch
Keyword(s):  
Nitric Oxide ◽  
G Protein ◽  
Signaling Proteins ◽  
Receptor Desensitization ◽  
Receptor Kinase ◽  
G Protein Coupled Receptor ◽  
Receptor Inactivation ◽  
Cardiac Regulation ◽  
G Protein Coupled ◽  
Signaling Components

Cardiac diseases including heart failure (HF), are the leading cause of morbidity and mortality globally. Among the prominent characteristics of HF is the loss of β-adrenoceptor (AR)-mediated inotropic reserve. This is primarily due to the derangements in myocardial regulatory signaling proteins, G protein-coupled receptor (GPCR) kinases (GRKs) and β-arrestins (β-Arr) that modulate β-AR signal termination via receptor desensitization and downregulation. GRK2 and β-Arr2 activities are elevated in the heart after injury/stress and participate in HF through receptor inactivation. These GPCR regulators are modulated profoundly by nitric oxide (NO) produced by NO synthase (NOS) enzymes through S-nitrosylation due to receptor-coupled NO generation. S-nitrosylation, which is NO-mediated modification of protein cysteine residues to generate an S-nitrosothiol (SNO), mediates many effects of NO independently from its canonical guanylyl cyclase/cGMP/protein kinase G signaling. Herein, we review the knowledge on the NO system in the heart and S-nitrosylation-dependent modifications of myocardial GPCR signaling components GRKs and β-Arrs.

Vanadium compounds cause activation of G protein-coupled receptor signaling

2020 ◽  
Author(s):  
Debbie C. Crans ◽  
Duaa Althumairy ◽  
Heide Murakami ◽  
B. George Barisas ◽  
Deborah Roess
Keyword(s):  
G Protein ◽  
Receptor Signaling ◽  
G Protein Coupled Receptor ◽  
Vanadium Compounds ◽  
G Protein Coupled
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