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首页> 外文期刊>Molecular and Cellular Biology >Processing of p60v-src to its myristylated membrane-bound form.
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Processing of p60v-src to its myristylated membrane-bound form.

机译：将p60v-src加工成肉豆蔻酰化的膜结合形式。

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p60src of wild-type Rous sarcoma virus is myristylated at its N-terminal glycine residue. We have shown previously that this myristylation is necessary for p60src membrane association and for cell transformation by using src mutants with alterations within the N-terminal 30 kilodaltons of p60src. In this study we analyzed the process of p60src myristylation in wild type- and mutant-infected cells. All myristylated src proteins examined lack the initiator methionine, but two mutant src proteins lacking the initiator methionine are not myristylated, indicating that removal of the initiator methionine and myristylation are not obligatorily coupled. Analysis of the kinetics of myristylation and the association of p60src with cellular proteins p50 and p90 indicated that myristylation occurs before p60src becomes membrane associated and that transient association with p50 and p90 occurs regardless of myristylation. Myristylation is required for stable association of p60src with the plasma membrane but is not sufficient for membrane association. A mutant with an src deletion of amino acids 169 through 264 has an src protein that is myristylated but not membrane bound, remaining stably associated with p50 and p90. This mutant is transformation defective. Several N-terminal deletion mutants possessing tyrosine kinase activity have myristylated and membrane-bound src proteins but are not fully active in cell transformation, suggesting that additional N-terminal functional domains exist.
机译：野生型劳斯肉瘤病毒的p60src在其N端甘氨酸残基上被肉豆蔻酰化。以前我们已经表明，这种肉豆蔻酰化对于p60src膜缔合和细胞转化是必需的，通过使用src突变体在p60src的N末端30千吨内具有改变。在这项研究中，我们分析了野生型和突变体感染的细胞中p60src肉豆蔻酰化的过程。检查的所有肉豆蔻酰化的src蛋白都缺少引发剂蛋氨酸，但是两个缺少引发剂蛋氨酸的突变src蛋白却没有被肉豆蔻化，这表明引发剂蛋氨酸的去除和肉豆蔻酰化不是强制性的。对肉豆蔻酰化的动力学以及p60src与细胞蛋白p50和p90缔合的分析表明，肉豆蔻酰化发生在p60src成为膜缔合之前，并且与p50和p90的瞬时缔合与肉豆蔻酰化无关。肉豆蔻化是p60src与质膜稳定缔合所必需的，但不足以实现膜缔合。具有从氨基酸169到264的src缺失的突变体具有一个src蛋白，该蛋白被肉豆蔻酰化，但未与膜结合，与p50和p90稳定结合。该突变体是转化缺陷的。几个具有酪氨酸激酶活性的N末端缺失突变体具有肉豆蔻酰化和膜结合的src蛋白，但在细胞转化中并不完全活跃，表明存在其他N末端功能域。

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