生物
髓系白血病
融合转录本
互补DNA
融合蛋白
染色体易位
基因
分子生物学
遗传学
内含子
融合基因
打开阅读框
嵌合基因
断点
基因表达
肽序列
癌症研究
重组DNA
作者
Marieke von Lindern,Maarten Fornerod,Sjozèf van Baal,Martine Jaegle,Ton de Wit,Arjan Buijs,Gerard C. Grosveld
标识
DOI:10.1128/mcb.12.4.1687-1697.1992
摘要
The translocation (6;9) is associated with a specific subtype of acute myeloid leukemia (AML). Previously, it was found that breakpoints on chromosome 9 are clustered in one of the introns of a large gene named Cain (can). cDNA probes derived from the 3' part of can detect an aberrant, leukemia-specific 5.5-kb transcript in bone marrow cells from t(6;9) AML patients. cDNA cloning of this mRNA revealed that it is a fusion of sequences encoded on chromosome 6 and 3' can. A novel gene on chromosome 6 which was named dek was isolated. In dek the t(6;9) breakpoints also occur in one intron. As a result the dek-can fusion gene, present in t(6;9) AML, encodes an invariable dek-can transcript. Sequence analysis of the dek-can cDNA showed that dek and can are merged without disruption of the original open reading frames and therefore the fusion mRNA encodes a chimeric DEK-CAN protein of 165 kDa. The predicted DEK and CAN proteins have molecular masses of 43 and 220 kDa, respectively. Sequence comparison with the EMBL data base failed to show consistent homology with any known protein sequences.
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