| As2O3诱导K562细胞凋亡过程中酪氨酸蛋白激酶活性的变化 |
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| 引用本文： | 肖冬梅,孙关林,邬维礼.As2O3诱导K562细胞凋亡过程中酪氨酸蛋白激酶活性的变化[J].中华血液学杂志,1998,19(5):234-236. |
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| 作者姓名： | 肖冬梅 孙关林 邬维礼 |
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| 作者单位： | 上海第二医科大学附属瑞金医院，上海血液学研究所 |
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| 基金项目： | 国家“九五”科技攻关项目基金,胡应洲部分基金 |
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| 摘 要： | 目的：阐明Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡的可能机制，为Ａｓ２Ｏ３治疗白血病的推广应用提供一定的理论基础。方法：采用免疫沉淀、Ｗｅｓｔｅｒｎｂｌｏｔ及生物化学等方法，观察在Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡过程中，细胞胞浆和胞膜蛋白及ＡＢＬ蛋白酪氨酸激酶（ＰＴＫ）活性及某些内源性蛋白酪氨酸磷酸化的变化。结果：在Ａｓ２Ｏ３诱导Ｋ５６２细胞凋亡过程中，细胞胞浆和胞膜蛋白及ＡＢＬ蛋白ＰＴＫ活性降低，分子量为１８万和１２．５万的蛋白酪氨酸磷酸化减少。结论：Ａｓ２Ｏ３可能通过降低细胞内某些蛋白，尤其ＢＣＲ／ＡＢＬ蛋白的ＰＴＫ活性，减少蛋白酪氨酸磷酸化，从而阻断ＢＣＲ／ＡＢＬ抗凋亡信号的传导，诱导Ｋ５６２细胞凋亡
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| 关 键 词： | 砷剂 蛋白酪氨酸激酶 细胞凋亡 |
Protein tyrosine kinase (PTK) activities during the induction of apoptosis by arsenic trioxide (As_2O_3) |
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| D Xiao,G Sun,W Wu.Protein tyrosine kinase (PTK) activities during the induction of apoptosis by arsenic trioxide (As_2O_3)[J].Chinese Journal of Hematology,1998,19(5):234-236. |
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| Authors: | D Xiao G Sun W Wu |
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| Affiliation: | Shanghai Institute of Hematology, Ruijin Hospital, Shanghai Second Medical University, Shanghai 200025. |
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| Abstract: | OBJECTIVE: To explore the mechanism of arsenic trioxide (As2O3) induced apoptosis in K562 cell line. METHODS: Immunoprecipitation was used to obtain BCR/ABL and ABL proteins. The activities of PTK and tyrosine phosphorylation were measured by biochemical method and Western blot, respectively. RESULTS: As2O3 reduced the PTK activities of cytosol and membrane proteins and BCR/ABL and ABL proteins. The tyrosine phosphorylation of 180,000 and 125,000 proteins declined. CONCLUSION: As2O3 may interfere the signal transduction of BCR/ABL protein by reducing its PTK activity and induce K562 cell apoptosis. |
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| Keywords: | Arsenicals Protein tyrosine kinase Apoptosis |
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