去泛素化酶家族种类繁多,分布于人体多种器官及组织,是泛素-蛋白酶体途径的重要组成部分,精细调控真核细胞生物细胞内蛋白的降解。A20、CYLD、泛素特异性加工酶7等去泛素化酶通过与外异蛋白受体、Fas相关的死亡区蛋白、B细胞淋巴因子-3、核因子-KB抑制蛋白激酶等因子相互作用,可参与银屑病、皮肤基底细胞癌、皮肤鳞状细胞癌、皮肤附属器肿瘤、Kaposi肉瘤以及恶性黑素瘤等皮肤疾病的发生发展。探讨去泛素化酶作用机制,有助于为炎症及肿瘤性皮肤病提供新的治疗靶点。
There are a great variety of deubiquitinating enzymes (DUBs) distributed in multiple human tis sues and organs. As an important part of ubiquitin-proteasome pathway (UPP), DUBs can tightly control the degra dation of eukaryotic intracellular proteins. It has been revealed that some deubiquitinating enzymes such as A20, cylindromatosis (CYLD) and ubiquitin-speeific processing protease-7 (USP7) may take part in the occurrence and development of psoriasis, basal cell carcinoma, squamous cell carcinoma, cutaneous adnexal neoplasms, Kaposis sarcoma and malignant melanoma through interaction with ectodysplasin-A receptor (EDAR), Fas-assoeiated death domain-containing protein (FADD), B-cell leukemia/lymphoma 3 (Bcl-3), I kappa B kinase (IKK), and so on. Therefore, exploring the action mechanism of deubiquitinating enzymes will help to find new targets for the treat ment of inflammatory dermatoses and skin tumors.