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首页> 外文期刊>Molecular and Cellular Biology >Interactions between cell growth-regulating domains in the products of the adenovirus E1A oncogene.
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Interactions between cell growth-regulating domains in the products of the adenovirus E1A oncogene.

机译：腺病毒E1A癌基因产物中细胞生长调节域之间的相互作用。

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Among the various biological activities expressed by the products of the adenovirus E1A gene are the abilities to induce cellular DNA synthesis and proliferation in quiescent primary baby rat kidney cells. The functional sites for these activities lie principally within two regions of the E1A proteins: an N-terminal region and a small second region of approximately 20 amino acids further downstream. To study the biological functions of the first domain, we constructed an in-frame deletion of amino acid positions 23 through 107 of the E1A products. This deletion did not impede the ability of the E1A products to transactivate the adenovirus early region 3 promoter in a transient-expression assay in HeLa cells. The ability to induce DNA synthesis in quiescent baby rat kidney cells was, however, lost in the absence of these sequences. Deletion of the small second region induced a form of S phase in which DNA synthesis occurred in the apparent absence of controls required for the cessation of DNA synthesis and progression through the remainder of the cell cycle. These cells did not appear to accumulate in or before G2, and many appeared to have a DNA content greater than that in G2. The functions of both domains are required for production of transformed foci in a ras cooperation assay. Focus formation occurred, however, even when the two domains were introduced on two separate plasmids. This complementation effect appeared to require expression of both of the mutant proteins and did not appear to result merely from recombination at the DNA level.
机译：腺病毒E1A基因产物表达的各种生物活性中，有一种能够在静止的原代幼鼠肾细胞中诱导细胞DNA合成和增殖。这些活性的功能位点主要位于E1A蛋白的两个区域内：一个N末端区域和一个更下游的约20个氨基酸的第二小区域。为了研究第一个结构域的生物学功能，我们构建了E1A产品第23至107位氨基酸的框内缺失。在HeLa细胞的瞬时表达测定中，该删除不妨碍E1A产物反式激活腺病毒3区早期启动子的能力。然而，在缺少这些序列的情况下，诱导了在静止的幼鼠肾细胞中诱导DNA合成的能力。小第二区域的缺失诱导了一种S相形式，其中DNA合成发生在明显缺乏控制DNA合成和在细胞周期其余部分中进行所需的对照的情况下。这些细胞似乎没有在G2之前或之前积累，并且许多DNA的含量似乎高于G2。在ras合作测定中产生转化的病灶需要两个域的功能。然而，即使将两个结构域引入两个单独的质粒中，也发生了焦点形成。这种互补作用似乎需要两种突变蛋白的表达，并且似乎并非仅由于DNA水平的重组而产生。

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