Identity between TRAP and SMCC complexes indicates novel pathways for the function of nuclear receptors and diverse mammalian activators
Identity between TRAP and SMCC complexes indicates novel pathways for the function of nuclear receptors and diverse mammalian activators
复制标题
DOI：
10.1016/s1097-2765(00)80463-3
复制
发表时间：
1999-03-01
期刊：
影响因子：
16
通讯作者：
Roeder, RG
中科院分区：
文献类型：
--
作者：
Ito, M;Yuan, CX;Roeder, RG
人甲状腺激素受体相关蛋白（TRAP）复合物，一种早期描述的核受体的共激活因子，以及一种介导Ga 14-p53激活的含SRB和MED的辅因子复合物（SMCC），在特定的多肽亚基、共激活因子功能和作用机制（激活因子相互作用）方面几乎相同。与TRAP 220亚基的核受体的配体依赖性相互作用平行，p53和VP 16激活结构域直接与新克隆的TRAP 80亚基相互作用。这些结果表明，新的途径的核受体和其他激活剂（p53和VP 16）的功能，通过一个共同的辅激活因子复合物，很可能靶向RNA聚合酶II。TRAP 230亚基作为先前预测的基因产物的鉴定也表明在某些疾病状态中存在与共激活因子相关的转录缺陷。
The human thyroid hormone receptor-associated protein (TRAP) complex, an earlier described coactivator for nuclear receptors, and an SRB- and MED-containing cofactor complex (SMCC) that mediates activation by Ga14-p53 are shown to be virtually the same with respect to specific polypeptide subunits, coactivator functions, and mechanisms of action (activator interactions). In parallel with ligand-dependent interactions of nuclear receptors with the TRAP220 subunit, p53 and VP16 activation domains interact directly with a newly cloned TRAP80 subunit. These results indicate novel pathways for the function of nuclear receptors and other activators (p53 and VP16) through a common coactivator complex that is likely to target RNA polymerase II. Identification of the TRAP230 subunit as a previously predicted gene product also suggests a coactivator-related transcription defect in certain disease states.