Published online before print August 21, 2006, doi: 10.1161/01.HYP.0000237975.90870.eb
(Hypertension. 2006;48:534.)
© 2006 American Heart Association, Inc.
Brief Reviews |
Angiotensin II Signal Transduction Through Small GTP-Binding Proteins
Mechanism and Significance in Vascular Smooth Muscle Cells
From the Cardiovascular Research Center and Department of Physiology (H.O., H.S., H.N., S.D., S.E.), Temple University School of Medicine, Philadelphia, Pa; Department of Biochemistry (G.D.F.), Vanderbilt University School of Medicine, Nashville, Tenn; and the Department of Biomedical Sciences (E.D.M.), Division of Cardiovascular Biology, Meharry Medical College, Nashville, Tenn.
Correspondence to Satoru Eguchi, Cardiovascular Research Center; Temple University School of Medicine, 3420 N Broad St, Philadelphia, PA 19140. E-mail seguchi@temple.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Small GTP-binding proteins (G proteins) are monomeric G proteins with a low molecular weight of 20 to 40 kDa. A small G protein acts as a molecular switch that cycles between inactive GDP-bound and active GTP-bound forms. Thus far, >100 small G proteins have been identified in eukaryotes from yeast to humans. The small G proteins in this superfamily are structurally classified into
5 families: the Ras, Rho, Rab, Sar/Arf, and Ran families. In general, the Ras family mainly regulates gene expression, the Rho family regulates both cytoskeletal reorganization and gene expression, the Rab and Sar1/Arf families regulate intracellular vesicle trafficking, and the Ran family regulates nucleocytoplasmic transport and microtubule organization during the cell cycle.1
Multiple downstream effectors of small G proteins, some of them being protein kinases, have been identified. Ras mediates its effect on cell proliferation mainly by activation of its effector Raf to initiate the mitogen-activated protein kinase (MAPK/extracellular signal regulated kinase [ERK]) cascade. In addition, a variety of Ras effectors have been identified, such as a phosphatidylinositol 3-kinase (PI3K). The Rho family, such as Rho, Rac, and Cdc42, also has various effectors. One of the Rho effectors, Rho-kinase (ROCK), plays an important role in actin cytoskeleton reorganization and smooth muscle contraction. In addition, reduced nicotinamide-adenine dinucleotide phosphate oxidase is known as a Rac effector and p70 S6 kinase (p70S6K) as a Cdc42 effector.1,2 Recently, small G proteins have been noted as novel therapeutic targets in cardiovascular medicine. In this regard, Ras and Rho G proteins are
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