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首页> 外文期刊>Molecular and Cellular Biology >Novel promoter upstream of the human c-myc gene and regulation of c-myc expression in B-cell lymphomas.
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Novel promoter upstream of the human c-myc gene and regulation of c-myc expression in B-cell lymphomas.

机译：人c-myc基因上游的新型启动子和B细胞淋巴瘤中C-myc表达的调节。

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A new promoter of the human c-myc gene called P0, with multiple RNA start sites, was mapped over 500 bases upstream of the two previously identified promoters, P1 and P2. Sequencing full-length cDNA clones of P0 RNAs revealed two open reading frames upstream of that for the P64c-myc protein. P0 RNA is located on polyribosomes and released by puromycin, indicating that it functions as an mRNA. In vitro translation of RNA synthesized from the cloned cDNAs predicts that P0 transcripts are translated into a novel 12.5-kilodalton protein corresponding to the first open reading frame. The regulation of P0 RNA was studied in the B-cell lymphoma cell line Manca, in which only the translocated c-myc allele lacking exon 1 was thought to be active. However, we found that P0 transcription and the DNase I-hypersensitive site associated with this promoter persist on the untranslocated allele, even though P1/P2 transcription as measured by a nuclear runoff assay was repressed. These results suggest that allelic exclusion of c-myc expression in this B-cell lymphoma is caused by a repression of transcription which is specific to the P1/P2 promoters. We previously reported a block to elongation of transcription near the 3' end of exon 1 in the wild-type c-myc gene, which results in an excess of exon 1 over exon 2 transcription (5a). In contrast, we found that in the Daudi B-cell lymphoma, which retains exon 1 in the active allele, equimolar transcription of exons 1 and 2 occurs. This result suggests a model for the activation of c-myc in B-cell lymphomas.
机译：具有多个RNA启动部位的人C-Myc基因的新启动子于两种先前鉴定的启动子，P1和P2上游映射了多个RNA开始部位。测序P0 RNA的全长cDNA克隆显示P64C-MYC蛋白的两个开放阅读框架。 P0 RNA位于多霉菌上并由嘌呤霉素释放，表明其用作mRNA。从克隆的CDNA合成的RNA的体外翻译预测，P0转录物被翻译成与第一开放阅读框相对应的新型12.5千杆杆菌蛋白。在B细胞淋巴瘤细胞系中研究了P0 RNA的调节，其中仅被认为是活跃的缺失的外显子1的转移的C-MYC等位基因。然而，我们发现P0转录和与该启动子相关的DNA酶I-过敏位点在未转化的等位基因上持续存在，即使通过核径流测定测量的P1 / P2转录被抑制。这些结果表明，在该B细胞淋巴瘤中的C-MyC表达等位基因排除是由对P1 / P2启动子特异的转录抑制引起的。我们之前报道了在野生型C-MYC基因中出现的3'末端附近的转录延伸的块，这导致过量的外显子1转录（5A）。相反，我们发现，在Daudi B细胞淋巴瘤中，其在活性等位基因中保持外显子1，发生外显子1和2的等摩尔转录。该结果表明B细胞淋巴瘤中C-MYC激活的模型。

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