Cullins and cancer.
Cullins and cancer.
复制标题
DOI：
10.1177/1947601910382899
复制
发表时间：
2010-07
期刊：
影响因子：
--
通讯作者：
Zhou P
中科院分区：
文献类型：
--
作者：
Lee J;Zhou P
泛素连接酶的cullin家族可以利用共享共同相互作用结构域的不同底物受体潜在地组装数百个RING型E3复合物（CRL）。Cullin受体决定底物特异性，并且Cullin介导的底物降解控制广泛的细胞过程，包括增殖、分化和凋亡。Cullin活性的失调已被证明有助于通过癌蛋白的积累或肿瘤抑制因子的过度降解的肿瘤发生。在这篇综述中，我们将讨论cullin复合物及其底物，影响cullin活性的调节途径，以及cullin可能促进或抑制致癌作用的机制。
The cullin family of ubiquitin ligases can potentially assemble hundreds of RING-type E3 complexes (CRLs) by utilizing different substrate receptors that share common interaction domains. Cullin receptors dictate substrate specificity, and cullin-mediated substrate degradation controls a wide range of cellular processes, including proliferation, differentiation, and apoptosis. Dysregulation of cullin activity has been shown to contribute to oncogenesis through the accumulation of oncoproteins or the excessive degradation of tumor suppressors. In this review, we will discuss cullin complexes and their substrates, the regulatory pathways that affect cullin activity, and the mechanisms by which cullins may facilitate or inhibit carcinogenesis.