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目的 :探讨原癌基因产物c CBL在P2 10BCR/ABL激发的异常信号转导中的作用。方法 :以慢性粒细胞白血病细胞株K56 2细胞为研究对象 ,用反义技术、免疫沉降和蛋白免疫印迹分析 ,研究c CBL、BCR/ABL和磷脂酰肌醇 3激酶 (phosphatidylinositol 3kinase ,PI3K)三者之间的相互关系。结果 :在K56 2细胞内 ,c CBL、BCR/ABL与PI3K可能形成一种三分子复合物 ,c cbl反义RNA转染细胞后BCR/ABL免疫沉降物中PI3K含量减少 59%左右 ,而BCR/ABL自身酪氨酸磷酸化水平无明显改变。结论 :原癌基因产物c CBL对BCR/ABL酪氨酸激酶活性无反向调节作用 ,它是连接BCR/ABL与PI3K之间的重要桥梁分子。
Objective: To investigate the role of proto-oncogene product c CBL in the abnormal signal transduction induced by P2 10BCR/ABL. METHODS: C562, CCR, BCR/ABL and phosphatidylinositol 3kinase (PI3K) were studied by using antisense technology, immunoprecipitation and Western blot analysis. The interrelationship between the two. RESULTS: In K562 cells, cCBL, BCR/ABL, and PI3K may form a three-molecule complex. After the c cbl antisense RNA transfected cells, the PI3K content in BCR/ABL immunoprecipitate was reduced by 59%. /ABL had no significant change in its tyrosine phosphorylation level. Conclusion : The proto-oncogene product c CBL has no reverse regulation of BCR/ABL tyrosine kinase activity. It is an important bridge between BCR/ABL and PI3K.