首页> 外文期刊>Molecular and Cellular Biology >N-terminal deletions in Rous sarcoma virus p60src: effects on tyrosine kinase and biological activities and on recombination in tissue culture with the cellular src gene.
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N-terminal deletions in Rous sarcoma virus p60src: effects on tyrosine kinase and biological activities and on recombination in tissue culture with the cellular src gene.

机译:劳斯肉瘤病毒p60src中的N端缺失:对酪氨酸激酶和生物学活性的影响以及对组织培养中细胞src基因重组的影响。

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We have constructed deletions within the region of cloned Rous sarcoma virus DNA coding for the N-terminal 30 kilodaltons of p60src. Infectious virus was recovered after transfection. Deletions of amino acids 15 to 149, 15 to 169, or 149 to 169 attenuated but did not abolish transforming activity, as assayed by focus formation and anchorage-independent growth. These deletions also had only slight effects on the tyrosine kinase activity of the mutant src protein. Deletion of amino acids 169 to 264 or 15 to 264 completely abolished transforming activity, and src kinase activity was reduced at least 10-fold. However, these mutant viruses generated low levels of transforming virus by recombination with the cellular src gene. The results suggest that as well as previously identified functional domains for p60src myristylation and membrane binding (amino acids 1 to 14) and tyrosine kinase activity (amino acids 250 to 526), additional N-terminal sequences (particularly amino acids 82 to 169) can influence the transforming activity of the src protein.
机译:我们已经构建了在克隆的劳斯肉瘤病毒DNA区域内编码p60src N末端30道尔顿的缺失。转染后恢复感染性病毒。如通过焦点形成和不依赖锚定的生长所测定的,氨基酸15至149、15至169或149至169的缺失被减弱,但是没有消除转化活性。这些删除也对突变的src蛋白的酪氨酸激酶活性仅有轻微的影响。氨基酸169至264或15至264的缺失完全消除了转化活性,并且src激酶活性降低了至少10倍。但是,这些突变病毒通过与细胞src基因重组产生了低水平的转化病毒。结果表明,除了先前确定的p60src肉豆蔻酰化和膜结合的功能域(氨基酸1至14)和酪氨酸激酶活性(氨基酸250至526)外,其他N端序列(尤其是氨基酸82至169)也可以影响src蛋白的转化活性。

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