The Akt kinase:: Molecular determinants of oncogenicity
The Akt kinase:: Molecular determinants of oncogenicity
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DOI：
10.1073/pnas.95.25.14950
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发表时间：
1998-12-08
影响因子：
11.1
通讯作者：
Vogt, PK
中科院分区：
文献类型：
--
作者：
Aoki, M;Batista, O;Vogt, PK
丝氨酸-苏氨酸激酶Akt是磷酸肌醇3-激酶（PI 3-激酶）的下游靶标;它被磷酸肌醇3-磷酸依赖性激酶PDK 1和PDK 2激活。某些突变形式的Akt诱导鸡胚成纤维细胞培养物中的致癌转化和幼鸡中的血管瘤。这种转化细胞的能力取决于Akt在质膜上的定位和Akt的激酶活性。Akt的反式显性负性形式干扰由编码PI 3-激酶的活化形式的p3 k癌基因诱导的致癌转化。因此，Akt是p3 k诱导的致癌性的重要介质。
The serine-threonine kinase Akt is a downstream target of phosphoinositide 3-kinase (PI 3-kinase); it is activated by the phosphoinositide 3-phosphate-dependent kinases PDK1 and PDK2. Certain mutated forms of Akt induce oncogenic transformation in chicken embryo fibroblast cultures and hemangiosarcomas in young chickens. This ability to transform cells depends on localization of Akt at the plasma membrane and on the kinase activity of Akt. A transdominant negative form of Akt interferes with oncogenic transformation induced by the p3k oncogene, which codes for an activated form of PI 3-kinase. Akt is therefore an essential mediator of p3k-induced oncogenicity.