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首页> 外文期刊>Cellular Physiology and Biochemistry >Impaired M_(3) Muscarinic acetylcholine receptor signal transduction through blockade of binding of multiple proteins to its third intracellular loop
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Impaired M_(3) Muscarinic acetylcholine receptor signal transduction through blockade of binding of multiple proteins to its third intracellular loop

机译：M_（3）毒蕈碱型乙酰胆碱受体信号转导受阻，通过阻止多种蛋白质与其第三胞内环的结合

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摘要

Several motifs found in the third intracellular loop of the M_(3) muscarinic receptor are critical for G protein activation and scaffold protein interaction. However, how multiprotein complexes form is not fully understood. A minigene encoding the third intracellular loop of the M_(3) muscarinic receptor was constructed to explore whether peptides from this intracellular region could act as inhibitors of the muscarinic multiprotein complex formation and signaling. We found that this construct, when co-expressed with the M_(3) receptor, has the ability to act as a competitive antagonist of G protein receptors and receptor-scaffold/accessory proteins. Transient transfection of human embryonic kidney-293 cells with DNA encoding the human M_(3) and M_(5) receptor subtypes results in a carbachol-dependent increase of inositol phosphate. Co-expression of the M_(3) third cytoplasmic loop minigene dramatically reduces both carbachol-mediated G protein activation and inositol phosphate accumulation. Minigene expression also abrogates activation of M_(3) and M_(5) receptor mitogen-activated protein kinases pathway. Furthermore, minigene expression led to reduced AKT activation. These data, together with results of co-immunoprecipitation of different scaffold and kinase proteins, provide experimental evidence for the role for the third cytoplasmic loop of the human M_(3) muscarinic receptor in G-protein activation and multiprotein complex formation.
机译：在M_（3）毒蕈碱受体的第三个细胞内环中发现的几个基序对于G蛋白激活和支架蛋白相互作用至关重要。但是，多蛋白复合物如何形成尚不完全清楚。构建了编码M_（3）毒蕈碱受体第三个胞内环的小基因，以探索来自该胞内区域的肽是否可以充当毒蕈碱多蛋白复合物形成和信号传导的抑制剂。我们发现，当与M_（3）受体共表达时，该构建体具有充当G蛋白受体和受体支架/附件蛋白的竞争性拮抗剂的能力。用编码人类M_（3）和M_（5）受体亚型的DNA瞬时转染人类胚胎肾293细胞会导致羧甲酚依赖性磷酸肌醇增加。 M_（3）第三胞质环小基因的共表达显着减少了卡巴胆碱介导的G蛋白激活和肌醇磷酸积累。小基因表达也废除了M_（3）和M_（5）受体有丝分裂原激活的蛋白激酶途径的激活。此外，小基因表达导致减少的AKT激活。这些数据，以及不同支架和激酶蛋白的免疫共沉淀结果，为人M_（3）毒蕈碱受体的第三胞质环在G蛋白活化和多蛋白复合物形成中的作用提供了实验证据。

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