Anthes J C, Billah M M, Cali A, Egan R W, Siegel M I
Biochem Biophys Res Commun. 1987 Jun 15;145(2):825-33. doi: 10.1016/0006-291x(87)91039-4.
Membranes prepared from DMSO-differentiated HL60 cells labeled with [3H]inositol hydrolyze polyphosphoinositides in a Ca2+-dependent manner, generating inositol 1,4-bisphosphate (IP2) and inositol 1,4,5-trisphosphate (IP3). Incubation of membranes with GTP or GTP gamma S reduces the concentration of Ca2+ required for activation. This nucleotide effect is potentiated by formyl-Met-Leu-Phe (FMLP). Pertussis toxin inhibits FMLP-induced augmentation, but not the induction of IP2/IP3 formation by GTP or GTP gamma S. These results suggest that differentiated HL60 cells contain a membrane-associated phospholipase C that degrades polyphosphoinositides and that activation of this enzyme is mediated by at least two guanine nucleotide binding proteins, one of which is linked to FMLP receptors and is pertussis toxin sensitive.
用[3H]肌醇标记的经二甲基亚砜（DMSO）分化的HL60细胞制备的细胞膜以Ca2+依赖的方式水解多磷酸肌醇，生成肌醇1,4-二磷酸（IP2）和肌醇1,4,5-三磷酸（IP3）。用GTP或GTPγS孵育细胞膜可降低激活所需的Ca2+浓度。甲酰甲硫氨酸亮苯丙氨酸（FMLP）可增强这种核苷酸效应。百日咳毒素抑制FMLP诱导的增强作用，但不抑制GTP或GTPγS诱导的IP2/IP3形成。这些结果表明，分化的HL60细胞含有一种与膜相关的磷脂酶C，它可降解多磷酸肌醇，并且该酶的激活至少由两种鸟嘌呤核苷酸结合蛋白介导，其中一种与FMLP受体相连且对百日咳毒素敏感。
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