Imoto M, Sujikai I, Ui H, Umezawa K
Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Yokohama, Japan.
Biochim Biophys Acta. 1993 Feb 24;1166(2-3):188-92. doi: 10.1016/0005-2760(93)90096-r.
Tyrosine kinase inhibitors such as erbstatin and lavendustin derivative inhibited platelet-derived growth factor (PDGF)- and bombesin-induced inositol phosphate formation and phospholipase C (PLC) activation in quiescent NIH3T3 cells. However, bombesin-induced PLC activation was only partially inhibited by tyrosine kinase inhibitors, whereas PDGF-induced activation was completely. Moreover, although bombesin-induced PLC activation was partially inhibited by pertussis toxin alone, this toxin inhibited almost completely in the presence of tyrosine kinase inhibitors. Thus, tyrosine kinase was suggested to be involved in PDGF- and bombesin-induced PLC activation in a different manner.
酪氨酸激酶抑制剂,如埃布他汀和拉文达斯汀衍生物,可抑制静止的NIH3T3细胞中血小板衍生生长因子(PDGF)和蛙皮素诱导的肌醇磷酸形成及磷脂酶C(PLC)激活。然而,蛙皮素诱导的PLC激活仅被酪氨酸激酶抑制剂部分抑制,而PDGF诱导的激活则被完全抑制。此外,虽然单独使用百日咳毒素可部分抑制蛙皮素诱导的PLC激活,但在酪氨酸激酶抑制剂存在的情况下,这种毒素几乎可完全抑制。因此,提示酪氨酸激酶以不同方式参与PDGF和蛙皮素诱导的PLC激活。