Yano K, Higashida H, Hattori H, Nozawa Y
FEBS Lett. 1985 Feb 25;181(2):403-6. doi: 10.1016/0014-5793(85)80301-x.
Studies were undertaken to further elucidate the mechanism(s) by which bradykinin-dependent phosphoinositide metabolism takes place in neuroblastoma X glioma hybrid NG108-15 cells [(1984) J. Biol. Chem. 259, 10201-10207] using [3H]inositol-labelled cells. Bradykinin produced net increases in the level of [3H]inositol phosphates, especially of [3H]inositol trisphosphate which is formed transiently and most rapidly. The results indicate that bradykinin activates a phosphodiesterase to break down phosphatidylinositol 4,5-bisphosphate, generating two recently recognized intracellular messengers, 1,2-diacylglycerol and inositol trisphosphate.
研究旨在进一步阐明缓激肽依赖性磷酸肌醇代谢在神经母细胞瘤X胶质瘤杂交细胞NG108-15中发生的机制[(1984年)《生物化学杂志》259卷,10201 - 10207页],使用[³H]肌醇标记的细胞。缓激肽使[³H]肌醇磷酸水平净增加,尤其是瞬时且最快速形成的[³H]肌醇三磷酸。结果表明缓激肽激活一种磷酸二酯酶以分解磷脂酰肌醇4,5 - 二磷酸,产生两种最近被认可的细胞内信使,1,2 - 二酰基甘油和肌醇三磷酸。