Brandt S J, Dougherty R W, Lapetina E G, Niedel J E
Proc Natl Acad Sci U S A. 1985 May;82(10):3277-80. doi: 10.1073/pnas.82.10.3277.
The binding of the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine to its cell surface receptor rapidly elicits the hydrolysis of phosphatidylinositol 4,5-bisphosphate by phospholipase C to form the putative second messengers inositol 1,4,5-trisphosphate and sn-1,2-diacylglycerol. To investigate the possible role of a guanine nucleotide binding protein in transduction of this membrane signal, we examined the effects of pertussis toxin on chemotactic peptide-stimulated inositol phospholipid metabolism in differentiated HL-60 cells labeled with [3H]inositol. Pertussis toxin inhibited the chemotactic tripeptide-stimulated production of inositol mono-, bis-, and trisphosphates and secretion of N-acetyl-beta-D-glucosaminidase in a time- and concentration-dependent manner. Treatment with pertussis toxin did not alter the total incorporation or the distribution of [3H]inositol in inositol phospholipid. Chemotactic peptide receptor number was unchanged, although a slight decrease in binding affinity was observed. These findings suggest a role for a guanine nucleotide binding protein in coupling the chemotactic peptide receptor to phospholipase C.
趋化肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸与其细胞表面受体的结合，能迅速引发磷脂酶C对磷脂酰肌醇4,5-二磷酸的水解，形成假定的第二信使肌醇1,4,5-三磷酸和sn-1,2-二酰基甘油。为了研究鸟嘌呤核苷酸结合蛋白在这种膜信号转导中的可能作用，我们检测了百日咳毒素对用[3H]肌醇标记的分化HL-60细胞中趋化肽刺激的肌醇磷脂代谢的影响。百日咳毒素以时间和浓度依赖性方式抑制趋化三肽刺激的肌醇单磷酸、双磷酸和三磷酸的产生以及N-乙酰-β-D-氨基葡萄糖苷酶的分泌。用百日咳毒素处理不会改变[3H]肌醇在肌醇磷脂中的总掺入量或分布。趋化肽受体数量没有变化，尽管观察到结合亲和力略有下降。这些发现表明鸟嘌呤核苷酸结合蛋白在将趋化肽受体与磷脂酶C偶联中起作用。
