Nourse J, Mellentin J D, Galili N, Wilkinson J, Stanbridge E, Smith S D, Cleary M L
Department of Pathology, Stanford University School of Medicine, California 94305.
Cell. 1990 Feb 23;60(4):535-45. doi: 10.1016/0092-8674(90)90657-z.
The gene (E2A) for enhancer binding transcription factors E12 and E47 maps to the t(1;19) chromosomal translocation breakpoint in pre-B cell leukemias. Altered E2A transcripts lacking sequences coding for the helix-loop-helix DNA binding motif were detected in several t(1;19)-carrying cell lines. Fusion cDNAs that crossed the t(1;19) breakpoint were cloned and shown to code for an 85 kd protein consisting of the amino-terminal two-thirds of E2A fused to a chromosome 1-derived protein. The fusion protein has the features of a chimeric transcription factor in which the DNA binding domain of E2A is replaced by the putative DNA binding domain of a homeoprotein from chromosome 1 for which the name Prl (pre-B cell leukemia) is proposed. Identical E2A-prl mRNA junctions were detected by PCR in three t(1;19)-carrying cell lines, indicating that the fusion transcripts and predicted chimeric protein are a consistent feature of this translocation.
增强子结合转录因子E12和E47的基因（E2A）定位于前B细胞白血病中t(1;19)染色体易位断点处。在多个携带t(1;19)的细胞系中检测到了缺失编码螺旋-环-螺旋DNA结合基序序列的E2A转录本。跨越t(1;19)断点的融合cDNA被克隆，并显示编码一种85 kd的蛋白质，该蛋白质由E2A氨基末端的三分之二与一种源自1号染色体的蛋白质融合而成。融合蛋白具有嵌合转录因子的特征，其中E2A的DNA结合结构域被来自1号染色体的一种同源蛋白的假定DNA结合结构域所取代，为此提出了Prl（前B细胞白血病）这一名称。通过PCR在三个携带t(1;19)的细胞系中检测到相同的E2A-prl mRNA连接，表明融合转录本和预测的嵌合蛋白是这种易位的一个一致特征。
