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小鼠c-myb癌基因的结构组织与核苷酸序列:ABPL肿瘤中的激活是由于病毒整合到一个内含子中,导致5'编码序列缺失。

Structural organization and nucleotide sequence of mouse c-myb oncogene: activation in ABPL tumors is due to viral integration in an intron which results in the deletion of the 5' coding sequences.

作者信息

Lavu S, Reddy E P

出版信息

Nucleic Acids Res. 1986 Jul 11;14(13):5309-20. doi: 10.1093/nar/14.13.5309.

Abstract

Bacteriophage libraries of mouse DNA were screened for sequences homologous to the v-myb oncogene and two overlapping clones containing the v-myb related region were isolated. Restriction enzyme mapping, heteroduplex analysis and nucleotide sequence analysis revealed the presence of nine exons. Six of these exons are homologous to the v-myb region while the other three exons are derived from the 5' region which is deleted in the viral oncogene. The sequences downstream to the sixth v-myb exon are not included in the 17 kbp of DNA sequences analyzed in this study. Comparison of the structure of the normal c-myb clone with its rearranged couterpart present in plasmacytoid lymphosarcomas revealed that the rearrangements occur in this locus as a result of viral integration. Present studies demonstrate that such a viral insertion interrupts the c-myb coding region at a region identical to that observed in the generation of the v-myb gene of avian myeloblastosis virus and results in the synthesis of mRNAs that lack the same 5' coding region.

摘要

从小鼠DNA的噬菌体文库中筛选与v-myb癌基因同源的序列,并分离出两个包含v-myb相关区域的重叠克隆。限制性内切酶图谱分析、异源双链分析和核苷酸序列分析显示存在九个外显子。其中六个外显子与v-myb区域同源,而另外三个外显子来自病毒癌基因中缺失的5'区域。本研究分析的17kbp DNA序列中不包括第六个v-myb外显子下游的序列。正常c-myb克隆的结构与其在浆细胞样淋巴肉瘤中存在的重排对应物的比较表明,重排是由于病毒整合在该位点发生的。目前的研究表明,这种病毒插入在与禽成髓细胞瘤病毒v-myb基因产生中观察到的相同区域中断了c-myb编码区,并导致合成缺乏相同5'编码区的mRNA。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e38e/311542/0d167a5a5235/nar00282-0194-a.jpg

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