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机构地区:[1]徐州市第一人民医院内科 [2]徐州医学院生物化学与分子生物学研究中心,徐州221002
出 处:《基础医学与临床》2000年第6期557-560,共4页Basic and Clinical Medicine
摘 要:热休克可以激活ERK,但信号传导的级联通路仍不清楚。我们的结果提示,在NIH3T3细胞中,热休克引起ERK活性升高是通过神经酰胺的代谢产生鞘氨醇,并伴随着Raf-1蛋白激酶的激活。但是,热休克和神经酰胺不能引起HL-60, U937和K562骨髓白血病细胞中ERK活性的升高。Heat shock can activate ERKs, but the signal pathw ay leading to ERKs activation by heat is unknown. Our results showed that in NI H3T3 cell the pathway of ERK activation by heat was via ceramide metabolism to s phingosine with stimulation of Raf-1 protein kinase. But heat shock and cerami de can not activate ERKs in myeloid leukemic cells cells (such as HL-60, U937 a nd K562 cells), suggesting that the deficiency in activating of ERK cascade appe ared to reside between ceramide generation and ERK activation.
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