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小鼠双微体2基因的基因组结构

Genomic organization of the mouse double minute 2 gene.

作者信息

Jones S N, Ansari-Lari M A, Hancock A R, Jones W J, Gibbs R A, Donehower L A, Bradley A

机构信息

Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Gene. 1996 Oct 10;175(1-2):209-13. doi: 10.1016/0378-1119(96)00151-5.

DOI:10.1016/0378-1119(96)00151-5
PMID:8917101
Abstract

Transfection of the mouse double minute 2 (Mdm2) oncogene has been found to induce immortalization of primary cells and to transform cultured cells. Amplification and/or overexpression of human MDM2 has been documented in a large percentage of human cancers. Mouse and human Mdm2 cDNA have been cloned from transformed cells and the cDNA sequence of both genes have been reported previously. In this report, we present the gene structure of mouse Mdm2. Comparison of the coding sequences of the Mdm2 gene with the previously reported cDNA sequence and with Mdm2 sequences obtained from an Mdm2-bearing cosmid clone capable of inducing transformation revealed that the reported cDNA sequence was in error, and that Mdm2-induced transformation of cells does not require an activating mutation in Mdm2. Ligation-anchor PCR analysis of transcripts produced from the P1 and P2 promoters indicates that transcription initiates at sites upstream of those reported previously for both promoters.

摘要

已发现转染小鼠双微体2(Mdm2)癌基因可诱导原代细胞永生化并转化培养细胞。在很大比例的人类癌症中已记录到人类MDM2的扩增和/或过表达。小鼠和人类Mdm2 cDNA已从转化细胞中克隆出来,并且这两个基因的cDNA序列先前已被报道。在本报告中,我们展示了小鼠Mdm2的基因结构。将Mdm2基因的编码序列与先前报道的cDNA序列以及从能够诱导转化的携带Mdm2的黏粒克隆获得的Mdm2序列进行比较,结果表明报道的cDNA序列有误,并且Mdm2诱导的细胞转化并不需要Mdm2中的激活突变。对由P1和P2启动子产生的转录本进行连接锚定PCR分析表明,转录起始于先前报道的两个启动子上游的位点。

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Genomic organization of the mouse double minute 2 gene.小鼠双微体2基因的基因组结构
Gene. 1996 Oct 10;175(1-2):209-13. doi: 10.1016/0378-1119(96)00151-5.
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Regulation of mdm2 expression by p53: alternative promoters produce transcripts with nonidentical translation potential.p53对mdm2表达的调控:不同启动子产生具有不同翻译潜能的转录本。
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The growth arrest function of the human oncoprotein mouse double minute-2 is disabled by downstream mutation in cancer cells.人类癌蛋白小鼠双微体2的生长抑制功能在癌细胞中因下游突变而丧失。
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Cloning, sequence analysis and expression of the cDNAs encoding the canine and equine homologues of the mouse double minute 2 (mdm2) proto-oncogene.编码小鼠双微体2(mdm2)原癌基因犬类和马类同源物的cDNA的克隆、序列分析及表达
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The mdm2 proto-oncogene.小鼠双微体2原癌基因
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Oncogene amplification in urothelial cancers with p53 gene mutation or MDM2 amplification.伴有p53基因突变或MDM2扩增的尿路上皮癌中的癌基因扩增。
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Translational enhancement of mdm2 oncogene expression in human tumor cells containing a stabilized wild-type p53 protein.在含有稳定野生型p53蛋白的人类肿瘤细胞中MDM2癌基因表达的翻译增强。
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NF-kappaB inhibits T-cell activation-induced, p73-dependent cell death by induction of MDM2.NF-κB 通过诱导 MDM2 抑制 T 细胞激活诱导的、p73 依赖性细胞死亡。
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Overexpression of Mdm2 in mice reveals a p53-independent role for Mdm2 in tumorigenesis.Mdm2在小鼠中的过表达揭示了Mdm2在肿瘤发生中不依赖p53的作用。
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