cAMP stimulation of acetylcholine receptor expression is mediated through posttranslational mechanisms.

When the four Torpedo acetylcholine receptor (AcChoR) subunit cDNAs are stably integrated into the genome of mouse fibroblast cells, alpha 2 beta gamma delta pentamers with proper pharmacological and electrophysiological properties are expressed on the cell surface. Expression of these AcChoRs can be regulated by agents that stimulate intracellular cAMP levels with the result that increased numbers of cell-surface AcChoRs are produced. Theophylline, 8-(4-chlorophenylthio)-adenosine 3':5'-cyclic monophosphate, cholera toxin, and forskolin stimulated AcChoR cell-surface expression 1.2-, 1.6-, 2.2-, and 2.3-fold, respectively. cAMP-stimulated expression is mediated through a posttranslational mechanism, and the observed increase in surface AcChoRs correlates with increased lifetimes of each newly synthesized subunit. Increased subunit lifetimes are not observed in cell lines expressing each subunit individually, indicating that subunit stabilization arises through heterologous subunit-subunit interactions. IMAGES:

当将4种电鳐来源的乙酰胆碱受体（AcChoR）亚基互补脱氧核糖核酸（cDNA）稳定整合至小鼠成纤维细胞基因组后，具备正确药理学与电生理特性的α2βγδ五聚体即可在细胞表面表达。此类乙酰胆碱受体的表达可被刺激细胞内环腺苷酸（cAMP）水平的试剂调控，最终使细胞表面的乙酰胆碱受体数量增加。其中，茶碱、8-(4-氯苯硫基)-腺苷3':5'-环一磷酸、霍乱毒素以及福司柯林，分别可使细胞表面乙酰胆碱受体的表达量提升1.2倍、1.6倍、2.2倍与2.3倍。由cAMP介导的受体表达上调通过翻译后机制实现，观测到的细胞表面乙酰胆碱受体数量增加与每个新合成亚基的半衰期延长呈正相关。而在仅单独表达各亚基的细胞系中，未观测到亚基半衰期延长的现象，这表明亚基稳定性的提升源自异源亚基间的相互作用。
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