The IgG3 subclass of β1-adrenergic receptor autoantibodies is an endogenous biaser of β1AR signaling-Reference-Cited by-同舟云学术

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

Published:2021-04-01 Issue:7 Volume:32 Page:622-633
ISSN:1059-1524
Container-title:Molecular Biology of the Cell
language:en
Short-container-title:MBoC

Author:

Mohan Maradumane L.¹,Nagatomo Yuji²,Saha Prasenjit Prasad¹,Mukherjee Sromona D.¹,Engelman Timothy¹,Morales Rommel¹,Hazen Stanley L.¹,Tang W. H. Wilson³,Prasad Sathyamangla V. Naga¹

Affiliation:

1. Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, and

2. Department of Cardiology, National Defense Medical College, Tokorozawa, Japan, 359-8513

3. Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic, Cleveland, OH 44195

Abstract

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.

Publisher

American Society for Cell Biology (ASCB)

Subject

Cell Biology,Molecular Biology

Reference48 articles.

1. Impact of human autoantibodies on β1-adrenergic receptor conformation, activity, and internalization

2. Mechanism of Action of Beta-Blocking Agents in Heart Failure

3. β-arrestin–biased signaling through the β2-adrenergic receptor promotes cardiomyocyte contraction

4. Autoantibodies Against the β1adrenoceptor from Patients with Dilated Cardiomyopathy Prolong Action Potential Duration and Enhance Contractility in Isolated Cardiomyocytes

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