GSBS Student Publications


Abolition of G protein inhibition of alpha 1A and alpha 1B calcium channels by co-expression of the beta 3 subunit

UMMS Affiliation

Graduate School of Biomedical Sciences; Department of Pharmacology; Program in Neuroscience



Document Type


Medical Subject Headings

Animals; Calcium Channels; Electrophysiology; Ethylmaleimide; GTP-Binding Proteins; Guanosine Diphosphate; Membrane Potentials; Microinjections; Oocytes; RNA, Complementary; Thionucleotides; Xenopus laevis


Life Sciences | Medicine and Health Sciences


Three different classes of alpha 1 Ca2+ channel (alpha 1A, alpha 1B, alpha 1C) were expressed in Xenopus oocytes to determine whether G protein-mediated inhibition is an inherent property of the alpha 1 subunit itself, and if so, whether co-expression of auxiliary subunits modulates the inhibition seen. From our data it is apparent that either alpha 1A or alpha 1B Ca2+ channels expressed alone are sufficient for voltage-dependent G protein inhibition. alpha 1C Ca2+ channels expressed alone do not exhibit the G protein inhibition seen in alpha 1A and alpha 1B channels. Additionally, co-expression of the beta 3 subunit abolishes the ability of G proteins to inhibit currents through alpha 1A and alpha 1B Ca2+ channels. Differential sensitivity of alpha 1 as well as modulation of properties by beta 3 provide a potential mechanism for the regulation of G protein-mediated inhibition in neurons.

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Citation: FEBS Lett. 1995 Aug 28;371(1):43-6.

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Link to Article in PubMed

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FEBS letters

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