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REGULATION OF SV40 GENE EXPRESSION

REGULATION OF SV40 GENE EXPRESSION
SV40基因表达的调控
批准号:
3939643
负责人:
J BRADY
金额:
$0.0万
依托单位国家:
美国
项目类别:
财政年份:
--
资助国家:
美国
项目状态:
未结题
起止时间:
至

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中文摘要
翻译
猴病毒40(SV40)有两个早期转录单位,分别是 从复制起点附近的区域转录而来。这个 早期-早期(EE)转录单位,其RNA编码一个大的T- 抗原和小T抗原,在术后早期占主导地位 感染。晚期-早期(LE)转录单位RNA起始 站点位于EE Tata Box的上游,其功能位于 感染后较晚时间。我们已经确定了体外培养的 SV40早-早(EE)和两个晚-早的翻译效率 早期(LE)RNA。我们证明了一个或一个的存在 AUG启动子前导序列中的两个潜在密码子 LE RNAs抑制下游T-RNA的有效翻译 抗原起始剂,8月。此外,le RNA的翻译 导致合成新的病毒蛋白,大小为2.7kD。这个 这种蛋白质的作用目前正在研究中。羧基 T抗原末端突变导致的T细胞数量下降幅度很小。 病毒DNA复制的效率但低于适当的 条件显著降低了传染性病毒的产量。 粒子数量增加了三个数量级。我们的研究已经 证明了病毒晚期RNA的减少在一定程度上是 对这些突变体在CV中产生的较低效价负责 1p细胞。此外,我们已经证明了病毒晚期 感染病毒的CV-1P细胞不产生未知蛋白 C末端突变体。这表明T抗原在多种疾病中起作用。 不可知蛋白的翻译。
英文摘要
Simian virus 40 (SV40) has two early transcriptional units that are transcribed from a region near the origin of replication. The early-early (EE) transcription unit, whose RNA encodes a large T- antigen and small t-antigen, predominates at early times post infection. The late-early (LE) transcription unit RNA initiation sites are located upstream of the EE TATA box and function at late time post infection. We have characterized the in vitro translational efficiency of SV40 early-early (EE) and two late- early (LE) RNAs. We demonstrated that the presence of one or two potential AUG initiator codons in the leader sequences of the LE RNAs inhibits efficient translation from the downstream T- antigen initiator, AUG. In addition, translation of the LE RNA resulted in the synthesis of new viral proteins, 2.7 Kd in size. The role of this protein is currently under investigation. Carboxy terminal mutants of T-antigen cause a minimal decrease in the efficiency of viral DNA replication but under appropriate conditions significantly decrease the yield of infectious virus particles by three orders of magnitude. Our studies have demonstrated that a reduction in viral late RNA is, in part, responsible for the lower titers produced by these mutants in CV- 1P cells. Furthermore, we have demonstrated that the viral late protein, agnoprotein, is not produced in CV-1P cells infected with C-terminal mutants. This suggest that T-antigen plays a role in the translation of agnoprotein.
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