Cullin3/KCTD5 induces monoubiquitination of ΔNp63α and impairs its activity
Cullin3/KCTD5 induces monoubiquitination of ΔNp63α and impairs its activity
复制标题
Cullin3/KCTD5 诱导 αNp63α 的单泛素化并损害其活性
DOI：
10.1002/1873-3468.13104
复制
发表时间：
2018-07-01
期刊：
影响因子：
3.5
通讯作者：
Li, Chenghua
中科院分区：
文献类型：
--
作者：
He, Hanbing;Peng, Yougong;Li, Chenghua
含有 5 (KCTD5) 的钾通道四聚化结构域先前被记录为 Cullin3-RING 连接酶 (CRL3) 的组成部分。据报道，KCTD5 可以诱导多聚泛素化蛋白的富集，而基于 KCTD5 的 CRL3 会破坏多种蛋白的稳定性。在我们目前的研究中，我们报告 KCTD5 可能与 p53 家族成员 Delta Np63 α 发生物理相互作用。我们的进一步研究表明，Cullin3/KCTD5 可以诱导 Delta Np63 α 的单泛素化。 Cullin3/KCTD5 下调 Delta Np63 α 的 DNA 结合亲和力，损害其反式活性或反式抑制活性。从功能上来说。 Cullin3/KCTD5 减弱 Delta Np63 α 的增殖活性。这些发现表明，基于 KCTD5 的 CRL3 可能介导单泛素化，并且是 Delta Np63 α 的新型调节因子。
Potassium channel tetramerization domain containing 5 (KCTD5) was previously documented as a component of the Cullin3-RING ligase (CRL3). It has been reported that KCTD5 can induce enrichment of polyubiquitinated proteins, and KCTD5-based CRL3 destabilizes several proteins. In our present study, we report that KCTD5 may physically interact with Delta Np63 alpha, which is a member of the p53 family. Our further investigation revealed that Cullin3/ KCTD5 can induce monoubiquitination of Delta Np63 alpha. Cullin3/KCTD5 downregulates the DNA-binding affinity of Delta Np63 alpha impairing either its transactivity or its transinhibitory activity. Functionally. Cullin3/KCTD5 abates the proproliferation activity of Delta Np63 alpha. These findings suggest that KCTD5-based CRL3 may mediate monoubiquitination and is a novel regulator of Delta Np63 alpha.