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Regulation of Ionic Channels by G Proteins

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Cellular and Molecular Mechanisms in Hypertension

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 308))

Abstract

Signals may flow through membranes by a pathway composed of three elements: receptor, G protein and effector. At present we know of about 80 different receptors, about 15 different G proteins and about 15 different effectors (1,2). The primary structures of noradrenergic, dopamine, 5-hydroxytryptamine and rhodopsin receptors are similar indicating that the receptors form a family (2). The predicted secondary structures have seven membrane spanning a helices with the greatest differences among receptors occurring in the cytoplasmic linkers (3). The G proteins also form a family in which heterogeneity resides largely in the a subunits for which some 15 different cDNAs have been described (4,2). Two to four forms of the β subunit have been described and there are at least three forms of the y subunit (4,2). By contrast, the effectors are quite different from each other and there appears to be no homology among adenylyl cyclase (AC) (4), cGMP phosphodiesterase (PDE) and voltage-dependent ionic channels (5,6), although the predicted secondary structures of AC and voltage-gated channels are similar. Within this group, voltage-gated channels clearly are a family (7).

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Authors and Affiliations

  1. Departments of Molecular Physiology and Biophysics, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, 77030, USA

    A. M. Brown, A. Yatani, G. Kirsch, A. M. J. VanDongen, B. Schubert & L. Birnbaumer

  2. Departments of Cell Biology, Baylor College of Medicine, One Baylor Plaza, Houston, Texas, 77030, USA

    J. Codina & L. Birnbaumer

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  1. A. M. Brown
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  2. A. Yatani
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  1. Bockus Research Institute, The Graduate Hospital and Department of Physiology, The University of Pennsylvania, 19104, Philadelphia, PA, USA

    Robert H. Cox

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Brown, A.M. et al. (1991). Regulation of Ionic Channels by G Proteins. In: Cox, R.H. (eds) Cellular and Molecular Mechanisms in Hypertension. Advances in Experimental Medicine and Biology, vol 308. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-6015-5_10

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