摘要
ＮＩＨ３Ｔ３细胞以劳氏肉瘤病毒（ＲＳＶ）经温度敏感突变株转染形成的细胞株ｔｓＬＡ９０，细胞在非允许温度（４０℃）时为正常表型，在允许温度（３３℃）下为转化表型；４０℃时，微丝分布发达，从４０℃移至３３℃１ｈ，微丝完全解聚，同时，其外基质成分纤粘蛋白（ＦＮ）亦相伴解聚。若在４０℃以外源性ＦＮ或对蛋白激酶Ｃ（ＰＫＣ）具有抑制作用的三氟拉嗪进行预处理后，再转入３３℃时便能抑制微丝的解聚。结果提示，除ＲＳＶｓｒｃ基因产物ＰＰ６０Ｖｓｒｃ外，ＰＫＣ及ＦＮ亦可能参与转化过程中对微丝组装的调节。
The tsLA90 cells which are NIH3T3 cells infected with a temperaturesensitive mutant of RSV were used in this experiment. Temperature downshift from restrictive (40℃) to permissive (33 ℃) conditions showed malignant phenotype in cultured cells. After temperature downshift for 1 h the microfilaments (MF) and fibronection (FN) fibers were disappeared. However,after treatment with trifluoperazine (TFP) for 24h. The distribution of MF in cells cultured at 33℃ was restored. It is noteworthy that at 40 ℃ the pretreatment with FN or TFP which also is one of inhibitors of protein kinase C (PKC),inhibited depolymerization of actin filaments after temperature downshift. The data suggest that the PKC and FN may be also involved in account for modulation of polymerization of actin filaments in processes of transformation of tsLA90 cells.
出处
《北京师范大学学报（自然科学版）》
CAS
CSCD
1994年第3期415-419,共5页
Journal of Beijing Normal University(Natural Science)
基金
国家自然科学基金
关键词
tsLA90细胞
细胞转化
微丝
解聚
tsLA90 cells
cell transformation
microfilament
trifluoperazine
fibronectin
