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环孢素A通过p38丝裂原活化蛋白激酶和细胞外信号调节激酶途径诱导K562细胞向红系分化。

Cyclosporin A induces erythroid differentiation of K562 cells through p38 MAPK and ERK pathways.

作者信息

Sawafuji Kanoko, Miyakawa Yoshitaka, Kizaki Masahiro, Ikeda Yasuo

机构信息

Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan.

出版信息

Am J Hematol. 2003 Jan;72(1):67-9. doi: 10.1002/ajh.10245.

Abstract

We studied the effects of cyclosporin A (CsA) on the erythroid differentiation of human erythroid leukemia cell line K562. After K562 was treated with CsA for 4 days, the percentage of hemoglobinized cells was increased by 3.3 times. Because it was reported p38 MAPK (p38) and ERK are involved in erythropoietin-induced erythroid differentiation, we studied their roles using specific inhibitors. p38 inhibitor (SB203580) prevented CsA-induced hemoglobin synthesis in K562 cells, although MEK/ERK inhibitor (U0126) enhanced it by 3.3 times in K562 cells. These results indicate activation of p38 and inactivation of ERK are involved in CsA-induced erythroid differentiation of K562 cells.

摘要

我们研究了环孢素A(CsA)对人红白血病细胞系K562红系分化的影响。用CsA处理K562细胞4天后,血红蛋白化细胞的百分比增加了3.3倍。由于有报道称p38丝裂原活化蛋白激酶(p38)和细胞外信号调节激酶(ERK)参与促红细胞生成素诱导的红系分化,我们使用特异性抑制剂研究了它们的作用。p38抑制剂(SB203580)可阻止CsA诱导K562细胞中的血红蛋白合成,而MEK/ERK抑制剂(U0126)在K562细胞中可使其增强3.3倍。这些结果表明,p38的激活和ERK的失活参与了CsA诱导的K562细胞红系分化。

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