Suppr超能文献

细胞密度反应元件对转铁蛋白受体1转录的抑制作用。

Inhibition of transferrin receptor 1 transcription by a cell density response element.

作者信息

Wang Jian, Chen Guohua, Pantopoulos Kostas

机构信息

Lady Davis Institute for Medical Research, Sir Mortimer B. Davis Jewish General Hospital, 3755 Cote-Ste-Catherine Road, Montreal, Quebec, Canada H3T 1E2.

出版信息

Biochem J. 2005 Dec 1;392(Pt 2):383-8. doi: 10.1042/BJ20050492.

Abstract

TfR1 (transferrin receptor 1) mediates the uptake of transferrin-bound iron and thereby plays a critical role in cellular iron metabolism. Its expression is coupled to cell proliferation/differentiation and controlled in response to iron levels and other signals by transcriptional and post-transcriptional mechanisms. It is well established that TfR1 levels decline when cultured cells reach a high density and in the present study we have investigated the underlying mechanisms. Consistent with previous findings, we demonstrate that TfR1 expression is attenuated in a cell-density-dependent manner in human lung cancer H1299 cells and in murine B6 fibroblasts as the result of a marked decrease in mRNA content. This response is not associated with alterations in the RNA-binding activity of iron regulatory proteins that are indicative of a transcriptional mechanism. Reporter assays reveal that the human TfR1 promoters contains sequences mediating cell-density-dependent transcriptional inhibition. Mapping of the human and mouse TfR1 promoters identified a conserved hexa-nucleotide 5'-GAGGGC-3' motif with notable sequence similarity to a previously described element within the IGF-2 (insulin-like growth factor-2) promoter. We show that this motif is necessary for the formation of specific complexes with nuclear extracts and for cell-density-dependent regulation in reporter gene assays. Thus the TfR1 promoter contains a functional 'cell density response element' (CDRE).

摘要

转铁蛋白受体1(TfR1)介导结合转铁蛋白的铁的摄取,因此在细胞铁代谢中起关键作用。其表达与细胞增殖/分化相关联,并通过转录和转录后机制响应铁水平及其他信号而受到调控。众所周知,当培养细胞达到高密度时,TfR1水平会下降,在本研究中我们探究了其潜在机制。与先前的研究结果一致,我们证明在人肺癌H1299细胞和小鼠B6成纤维细胞中,TfR1表达以细胞密度依赖性方式减弱,这是mRNA含量显著降低的结果。这种反应与铁调节蛋白的RNA结合活性改变无关,而铁调节蛋白的RNA结合活性改变是转录机制的指示。报告基因检测显示,人TfR1启动子包含介导细胞密度依赖性转录抑制的序列。对人和小鼠TfR1启动子的定位鉴定出一个保守的六核苷酸5'-GAGGGC-3'基序,其与胰岛素样生长因子-2(IGF-2)启动子内先前描述的元件具有显著的序列相似性。我们表明,该基序对于与核提取物形成特异性复合物以及在报告基因检测中进行细胞密度依赖性调节是必需的。因此,TfR1启动子包含一个功能性的“细胞密度反应元件”(CDRE)。

相似文献

9
The activity of interleukin-4 receptor alpha-chain promoter is regulated by a GT box element.
Mol Immunol. 2006 Apr;43(11):1808-16. doi: 10.1016/j.molimm.2005.10.016. Epub 2005 Dec 7.

引用本文的文献

4
Hepatitis C virus infection causes iron deficiency in Huh7.5.1 cells.丙型肝炎病毒感染导致Huh7.5.1细胞出现缺铁。
PLoS One. 2013 Dec 13;8(12):e83307. doi: 10.1371/journal.pone.0083307. eCollection 2013.
7
Liver iron transport.肝脏铁转运
World J Gastroenterol. 2007 Sep 21;13(35):4725-36. doi: 10.3748/wjg.v13.i35.4725.

本文引用的文献

1
Iron metabolism and toxicity.铁代谢与毒性
Toxicol Appl Pharmacol. 2005 Jan 15;202(2):199-211. doi: 10.1016/j.taap.2004.06.021.
2
Transferrin receptor 1.转铁蛋白受体1
Int J Biochem Cell Biol. 2004 Nov;36(11):2137-43. doi: 10.1016/j.biocel.2004.02.007.
6
Role of Ets-1 in transcriptional regulation of transferrin receptor and erythroid differentiation.
Oncogene. 2002 Nov 14;21(52):7933-44. doi: 10.1038/sj.onc.1205925.
9
Regulation of ferritin genes and protein.铁蛋白基因与蛋白质的调控
Blood. 2002 May 15;99(10):3505-16. doi: 10.1182/blood.v99.10.3505.

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验