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通过脉冲场凝胶电泳分析发现,在经化学处理的人细胞系MNNG-HOS中,两个MET等位基因存在复杂的重排。

Analysis by pulsed field gel electrophoresis reveals complex rearrangements in two MET alleles in a chemically-treated human cell line, MNNG-HOS.

作者信息

Testa J R, Park M, Blair D G, Kalbakji A, Arden K, Vande Woude G F

机构信息

National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21701.

出版信息

Oncogene. 1990 Oct;5(10):1565-71.

PMID:2250912
Abstract

We have previously shown that two alleles of the MET locus are independently rearranged in the chemically-treated human cell line MNNG-HOS. One allele is the TPR-MET oncogene which was activated by fusion of the MET locus on chromosome 7 with the TPR locus on chromosome 1. The second allele is found on a der(7)t(1;7)(q23;q32) chromosome and is characterized by a deletion of the amino-terminus of the MET extracellular ligand binding domain. Here we present a pulsed field gel electrophoresis analysis which reveals that the two MET allele rearrangements in MNNG-HOS cells are more complex than originally thought. The breakpoint in MET on der(7) has been molecularly cloned and, unexpectedly, we found that rearrangement in this allele involves sequences derived from chromosome 2. Moreover, the rearrangement producing der(7) involves an inversion of the MET locus or a more complex alteration. Analysis of hybrid cells containing TPR-MET demonstrated that both the upstream and downstream portions of MET are conserved in this rearrangement and that oncogene activation occurred by an insertion of TPR sequences into the MET locus. These findings illustrate that when examined at the molecular level some chromosome abnormalities can be extremely complex and, thus, are of limited value in gene mapping studies.

摘要

我们之前已经表明,在经化学处理的人类细胞系MNNG-HOS中,MET基因座的两个等位基因发生了独立重排。一个等位基因是TPR-MET癌基因,它是通过7号染色体上的MET基因座与1号染色体上的TPR基因座融合而被激活的。第二个等位基因位于一条der(7)t(1;7)(q23;q32)染色体上,其特征是MET细胞外配体结合域的氨基末端缺失。在此,我们展示了一项脉冲场凝胶电泳分析,该分析揭示了MNNG-HOS细胞中两种MET等位基因重排比最初认为得更为复杂。der(7)上MET的断点已被分子克隆,出乎意料的是,我们发现该等位基因的重排涉及来自2号染色体的序列。此外,产生der(7)的重排涉及MET基因座的倒位或更复杂的改变。对含有TPR-MET的杂交细胞的分析表明,MET的上游和下游部分在这种重排中是保守的,并且癌基因激活是通过将TPR序列插入MET基因座而发生的。这些发现表明,在分子水平上进行检查时,一些染色体异常可能极其复杂,因此在基因定位研究中的价值有限。

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