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二甲基亚砜和血红素通过不同机制诱导小鼠红白血病细胞中的铁螯合酶mRNA。

Dimethyl sulphoxide and haemin induce ferrochelatase mRNA by different mechanisms in murine erythroleukaemia cells.

作者信息

Fukuda Y, Fujita H, Taketani S, Sassa S

机构信息

Rockefeller University, New York, NY 10021.

出版信息

Br J Haematol. 1993 Mar;83(3):480-4. doi: 10.1111/j.1365-2141.1993.tb04674.x.

DOI:10.1111/j.1365-2141.1993.tb04674.x
PMID:8485055
Abstract

The level of mRNA encoding ferrochelatase (FeC), the terminal enzyme of the haem biosynthetic pathway, was examined in murine erythroleukaemia (MEL) cells when they were induced to undergo erythroid cell differentiation by treatment with dimethyl sulphoxide (DMSO), or haemin. FeC mRNA increased within 12 h after DMSO or haemin treatment of MEL cells, and its level continued to increase for 48 h. Treatment of cells with succinylacetone (SA), a potent inhibitor of haem synthesis, suppressed a DMSO-mediated increase in FeC mRNA, and haemin treatment reversed a SA-mediated decrease in FeC mRNA. Nuclear runoff analyses showed that, while DMSO increased the rate of transcription of FeC mRNA, haemin did not. These results indicate that the induction of FeC mRNA by DMSO is largely transcriptional, while that by haemin is post-transcriptional.

摘要

在鼠类红白血病(MEL)细胞中,当用二甲基亚砜(DMSO)或血红素处理诱导其进行红细胞分化时,对血红素生物合成途径的末端酶——编码亚铁螯合酶(FeC)的mRNA水平进行了检测。在用DMSO或血红素处理MEL细胞后的12小时内,FeC mRNA增加,并且其水平在48小时内持续升高。用琥珀酰丙酮(SA)(一种血红素合成的有效抑制剂)处理细胞,抑制了DMSO介导的FeC mRNA增加,而血红素处理则逆转了SA介导的FeC mRNA减少。核转录分析表明,虽然DMSO增加了FeC mRNA的转录速率,但血红素没有。这些结果表明,DMSO对FeC mRNA的诱导主要是转录水平的,而血红素的诱导是转录后水平的。

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The ferrochelatase gene structure and molecular defects associated with erythropoietic protoporphyria.与红细胞生成性原卟啉症相关的亚铁螯合酶基因结构和分子缺陷。
J Bioenerg Biomembr. 1995 Apr;27(2):231-8. doi: 10.1007/BF02110038.