A-to-I RNA editing modulates the pharmacology of neuronal ion channels and receptors.
The regulation of neuronal excitability is complex, as ion channels and neurotransmitter receptors are underlying a large variety of modulating effects. Alterations in the expression patterns of receptors or channel subunits as well as differential splicing contribute to the regulation of neuronal excitability. RNA editing is another and more recently explored mechanism to increase protein diversity, as the genomic recoding leads to new gene products with novel functional and pharmacological properties. In humans A-to-I RNA editing targets several neuronal receptors and channels, including GluR2/5/6 subunits, the Kv1.1 channel, and the 5-HT(2C) receptor. Our review summarizes that RNA editing of these proteins does not only change protein function, but also the pharmacology and presumably the drug therapy in human diseases.
Institute for Physiology and Pathophysiology, Vegetative Physiology, Philipps University Marburg, Marburg, 35037, Germany.
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Decher
D000241:Adenosine / Q000235:genetics* / Q000378:metabolism; D000818:Animals; D006801:Humans; D007288:Inosine / Q000235:genetics* / Q000378:metabolism; D007473:Ion Channels / Q000235:genetics* / Q000378:metabolism; D009422:Nervous System Diseases / Q000188:drug therapy* / Q000235:genetics* / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D017393:RNA Editing; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism
D007473:Ion Channels; D018377:Neurotransmitter Agents; D011956:Receptors, Cell Surface; D007288:Inosine; D000241:Adenosine