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铁原卟啉IX(血红素)而非锡或锌原卟啉IX能够从含有NF-E2结合位点的增强子元件刺激K562细胞中的基因表达。

Iron protoporphyrin IX (hemin) but not tin or zinc protoporphyrin IX can stimulate gene expression in K562 cells from enhancer elements containing binding sites for NF-E2.

作者信息

Palma J F, Gao X, Lin C H, Wu S, Solomon W B

机构信息

Department of Medicine, State University of New York Health Science Center-Brooklyn 11203.

出版信息

Blood. 1994 Aug 15;84(4):1288-97.

PMID:8049443
Abstract

Many genes whose transcription is erythroid-specific contain enhancer or promoter elements that bind the transcription factor NF-E2. Hemin induction increases the expression of globin genes in the human erythroleukemia cell line K562, and increases the expression of reporters gene regulated by an enhancer elements containing binding sites for NF-E2. The failure of metalloporphyrins other than hemin to stimulate the transient expression of a CAT reporter gene linked to an enhancer element containing a binding site for NF-E2 was correlated with their failure to induce benzidine-positive K562 cells and increase the steady-state level of gamma-globin mRNA. This study suggests that elevated levels of zinc protoporphyrin IX found in the anemia of chronic disease, iron deficiency, and lead poisoning may contribute to a decrease in globin gene expression by interfering with the transcriptional activity of enhancer elements containing binding sites for NF-E2.

摘要

许多转录具有红系特异性的基因含有与转录因子NF-E2结合的增强子或启动子元件。血红素诱导可增加人红白血病细胞系K562中珠蛋白基因的表达,并增加由含有NF-E2结合位点的增强子元件调控的报告基因的表达。除血红素外的金属卟啉未能刺激与含有NF-E2结合位点的增强子元件相连的CAT报告基因的瞬时表达,这与它们未能诱导联苯胺阳性的K562细胞以及未能提高γ-珠蛋白mRNA的稳态水平相关。本研究表明,在慢性病贫血、缺铁和铅中毒中发现的锌原卟啉IX水平升高,可能通过干扰含有NF-E2结合位点的增强子元件的转录活性,导致珠蛋白基因表达降低。

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