Protein ubiquitination constitutes a post‐translational modification mediated by ubiquitin ligases whereby ubiquitinated substrates are degraded through the proteasomal or lysosomal pathways, or acquire novel molecular functions according to their “ubiquitin codes.” Dysfunction of the ubiquitination process in cells causes various diseases such as cancers along with neurodegenerative, auto‐immune/inflammatory, and metabolic diseases. KCTD10 functions as a substrate recognition receptor for cullin‐3 (CUL3), a scaffold protein in RING‐type ubiquitin ligase complexes. Recently, studies by ourselves and others have identified new substrates that are ubiquitinated by the CUL3/KCTD10 ubiquitin ligase complex. Moreover, the type of polyubiquitination (e.g., K27‐, K48‐, or K63‐chain) of various substrates (e.g., RhoB, CEP97, EIF3D, and TRIF) mediated by KCTD10 underlies its divergent roles in endothelial barrier formation, primary cilium formation, plasma membrane dynamics, cell proliferation, and immune response. Here, the physiological functions of KCTD10 are summarized and potential mechanisms are proposed.

中文翻译：

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KCTD10 生物学：泛素 E3 复合物的接头与多种底物相遇：cullin-3/KCTD10 E3 泛素连接酶复合物在各种细胞系中的不同作用。

蛋白质泛素化是由泛素连接酶介导的翻译后修饰，泛素化底物通过蛋白酶体或溶酶体途径降解，或根据其“泛素代码”获得新的分子功能。细胞中泛素化过程的功能障碍会导致各种疾病，例如癌症以及神经退行性疾病、自身免疫/炎症和代谢疾病。KCTD10 作为 cullin-3 (CUL3) 的底物识别受体起作用，CUL3 是 RING 型泛素连接酶复合物中的支架蛋白。最近，我们自己和其他人的研究已经确定了被 CUL3/KCTD10 泛素连接酶复合物泛素化的新底物。此外，各种底物（例如，RhoB、CEP97、EIF3D、和 TRIF) 介导的 KCTD10 是其在内皮屏障形成、初级纤毛形成、质膜动力学、细胞增殖和免疫反应中的不同作用的基础。在这里，总结了 KCTD10 的生理功能并提出了潜在的机制。