Cataldi A, Caracino A, Di Baldassarre A, Robuffo I, Miscia S
Istituto di Morfologia Umana Normale, Università G. D'Annunzio, Chieti, Italy.
Cell Signal. 1995 Aug;7(6):627-33. doi: 10.1016/0898-6568(95)00030-s.
The early molecular mechanisms activated by the treatment of human lymphocytes with human interferon beta have been studied. These identify an early increase with respect to control, in diacylglycerol (DG) levels as response to interferon treatment. Such a DG production was derived from the rapid and sequential activation of phosphoinositide specific phospholipase C and phospholipase D pathway. This suggests that a synergistic involvement of phosphatidylinositol-bis-phosphate (PIP2) hydrolysis and phosphatidylcholine (PC) breakdown provide early molecular events upon the interaction between interferon beta and its cell surface receptors. This finally leads to the slowing down of cell growth.
人们已经研究了用人类β干扰素治疗人类淋巴细胞所激活的早期分子机制。这些机制表明,作为对干扰素治疗的反应,二酰基甘油(DG)水平相对于对照组有早期升高。这种DG的产生源于磷酸肌醇特异性磷脂酶C和磷脂酶D途径的快速且相继激活。这表明磷脂酰肌醇-双磷酸(PIP2)水解和磷脂酰胆碱(PC)分解的协同作用在干扰素β与其细胞表面受体相互作用时提供了早期分子事件。这最终导致细胞生长减缓。