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剑尾鱼中由偶然获得的启动子实现的肿瘤抑制

Tumor suppression in Xiphophorus by an accidentally acquired promoter.

作者信息

Adam D, Dimitrijevic N, Schartl M

机构信息

Genzentrum, Max-Planck-Institut für Biochemie, Martinsried, Germany.

出版信息

Science. 1993 Feb 5;259(5096):816-9. doi: 10.1126/science.8430335.

DOI:10.1126/science.8430335
PMID:8430335
Abstract

Melanoma formation in the teleost Xiphophorus is caused by a dominant genetic locus, Tu. This locus includes the Xmrk oncogene, which encodes a receptor tyrosine kinase. Tumor induction is suppressed in wild-type fish by a tumor suppressor locus, R. Molecular genetic analyses revealed that the Tu locus emerged by nonhomologous recombination of the Xmrk proto-oncogene with a previously uncharacterized sequence, D. This event generated an additional copy of Xmrk with a new promoter. Suppression of the new Xmrk promoter by R in parental fish and its deregulation in hybrids explain the genetics of melanoma formation in Xiphophorus.

摘要

硬骨鱼剑尾鱼属中黑色素瘤的形成是由一个显性基因座Tu引起的。该基因座包含Xmrk原癌基因,它编码一种受体酪氨酸激酶。野生型鱼类中的肿瘤抑制基因座R可抑制肿瘤诱导。分子遗传学分析表明,Tu基因座是由Xmrk原癌基因与一个以前未鉴定的序列D通过非同源重组产生的。这一事件产生了带有新启动子的Xmrk额外拷贝。亲本鱼类中R对新Xmrk启动子的抑制及其在杂种中的失调解释了剑尾鱼属黑色素瘤形成的遗传学机制。

相似文献

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Tumor suppression in Xiphophorus by an accidentally acquired promoter.剑尾鱼中由偶然获得的启动子实现的肿瘤抑制
Science. 1993 Feb 5;259(5096):816-9. doi: 10.1126/science.8430335.
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The macromelanophore locus and the melanoma oncogene Xmrk are separate genetic entities in the genome of Xiphophorus.在剑尾鱼基因组中,大黑色素细胞基因座和黑色素瘤癌基因Xmrk是不同的遗传实体。
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The Xmrk receptor tyrosine kinase is activated in Xiphophorus malignant melanoma.Xmrk受体酪氨酸激酶在剑尾鱼恶性黑色素瘤中被激活。
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Genome Res. 1996 Feb;6(2):102-13. doi: 10.1101/gr.6.2.102.

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