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(Circulation. 1996;94:602-603.)
© 1996 American Heart Association, Inc.

Articles

Multifunctional G Proteins

Searching for Functions in the Heart

Gary L. Stiles, MD

the Division of Cardiology, Duke University Medical Center, Durham, NC.

Correspondence to Gary L. Stiles, MD, Duke University Medical Center, Box 3444, 405 Sands Bldg, Research Dr, Durham, NC 27710.

Key Words: Editorials • proteins • heart failure • receptors, adrenergic, alpha • signal transduction

	Introduction

 
Regulation of cell signaling pathways in pathophysiological conditions, such as ischemia or congestive heart failure, has been studied intensively for many decades. Much has been learned concerning how various receptors, guanine nucleotide–binding proteins (G proteins), and effector molecules, such as adenylyl cyclase or phospholipase C (PLC), are modulated in disease states.¹ We have learned that receptors can be upregulated and downregulated, receptor–G protein coupling can be perturbed, the quantity of G proteins can be influenced, and the ability to generate second messengers can be enhanced or reduced.¹ At one level, the accompanying article is simply another in a long line of studies showing how a particular receptor system, namely, the ₁-adrenergic receptor (AR), can be quantitatively modulated in some forms of congestive heart failure, such as ischemic cardiomyopathy, whereas the ₁-AR in dilated cardiomyopathy is not quantitatively controlled. In addition, the activity of the G protein to which the ₁-AR couples appears to be regulated in a significant manner but by different mechanisms in ischemic versus dilated cardiomyopathy. If this were the whole story, I would not have much else to say and probably would not even suggest that you read the accompanying article. However, this is not the entire story; the G protein (G_h) being studied in this case is a fascinating molecule, and the role it plays in cell regulation remains enigmatic.

G_h is a large, 74-kD protein (the more common G proteins, such as _s and _i, which stimulate or inhibit adenylyl cyclase, are all in the . . . [Full Text of this Article]

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