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• W1979466745 endingPage "1212" @default.
• W1979466745 startingPage "1201" @default.
• W1979466745 abstract "The functional roles subserved by G(alpha)z, a G protein alpha subunit found predominantly in neuronal tissues, have remained largely undefined. Here, we report that G(alpha)z coupled neurotransmitter receptors to N-type Ca2+ channels when transiently overexpressed in rat sympathetic neurons. The G(alpha)z-mediated inhibition was voltage dependent and PTX insensitive. Recovery from G(alpha)z-mediated inhibition was extremely slow but accelerated by coexpression with RGS proteins. G(alpha)z selectively interacted with a subset of receptors that ordinarily couple to N-type Ca2+ channels via PTX-sensitive Go/i proteins. In addition, G(alpha)z rescued the activation of heterologously expressed GIRK channels in PTX-treated neurons. These results suggest that G(alpha)z is capable of coupling receptors to ion channels and might underlie PTX-insensitive ion channel modulation observed in neurons under physiological and pathological conditions." @default.
• W1979466745 created "2016-06-24" @default.
• W1979466745 creator A5008649533 @default.
• W1979466745 creator A5076023837 @default.
• W1979466745 date "1998-11-01" @default.
• W1979466745 modified "2023-10-16" @default.
• W1979466745 title "G Protein α Subunit Gα z Couples Neurotransmitter Receptors to Ion Channels in Sympathetic Neurons" @default.
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• W1979466745 doi "https://doi.org/10.1016/s0896-6273(00)80636-4" @default.
• W1979466745 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9856474" @default.
• W1979466745 hasPublicationYear "1998" @default.
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