Cataldi A, Di Pietro R, Robuffo I, Di Baldassarre A, Miscia S
Istituto di Morfologia Umana Normale, Università G. D'Annunzio, Chieti, Italy.
Cell Struct Funct. 1994 Dec;19(6):375-84. doi: 10.1247/csf.19.375.
The modulation of phosphoinositidase C (PIC) beta activity upon interferon treatment in Burkitt lymphoma cells (Daudi) and its localization and expression have been analyzed by Western blotting, immunocytochemical and immunoelectronmicroscopy analysis. Results have disclosed an early increase of phosphatidyl-inositol-bisphosphate (PIP2) hydrolysis at nuclear level upon interferon (IFN) treatment paralleled by the evidence of an increase of PIC beta 1 expression. PIC beta 1 expression has been detected in the nuclear compartment also in a clone of Daudi cells selected for the resistance to the antiproliferative action of interferon alpha but no modulation of the enzyme has been detected upon interferon treatment. Since no changes in terms of PIP2 hydrolysis have been found at nuclear level in this selected line, we suggest that the antiproliferative action of interferon on Burkitt lymphoma cells is mediated by a possible recruitment of nuclear PIC beta 1 expression.
通过蛋白质免疫印迹、免疫细胞化学和免疫电子显微镜分析,对伯基特淋巴瘤细胞(Daudi细胞)经干扰素处理后磷脂酰肌醇酶C(PIC)β活性的调节及其定位和表达进行了分析。结果显示,干扰素(IFN)处理后,核水平上磷脂酰肌醇二磷酸(PIP2)水解早期增加,同时伴有PICβ1表达增加的证据。在对干扰素α抗增殖作用具有抗性的Daudi细胞克隆的核区室中也检测到了PICβ1表达,但经干扰素处理后未检测到该酶的调节。由于在该选定细胞系的核水平未发现PIP2水解方面的变化,我们认为干扰素对伯基特淋巴瘤细胞的抗增殖作用可能是由核PICβ1表达的可能募集介导的。