CYLD是抑癌基因，编码一种去泛素化酶，可以特异性地去除赖氨酸-63-连接的泛素标记。CYLD将下游的调节因子（例如：TRAF2和TRAF6）去泛素化来负向调节NF-κB信号。CYLD主要是通过抑制NF-κB通路和增强细胞凋亡来发挥肿瘤抑制作用。尽管CYLD具有公认的肿瘤抑制作用，但是CYLD还调节微管动力学并在细胞迁移和血管生成过程中发挥作用。CYLD参与其他生理过程，如免疫应答、炎症、细胞周期进程、精子生成和破骨细胞生成。CYLD突变在各种癌症中发生频率都比较低。大约25%的CYLD变异是截短突变。CYLD胚系突变与柱状瘤病、多发性家族性毛发上皮瘤、Brooke Spiegler综合征有关。

CYLD is a deubiquitinating enzyme that removes lysine-63-linked ubiquitin marks. It negatively regulates NF-κB signaling by deubiquitinating upstream regulators such as TRAF2 and TRAF6. CYLD has a tumor suppressor role, principally via NF-κB pathway inhibition and enhancement of apoptosis. Despite its recognized tumor suppressor role, CYLD also modulates microtubule dynamics and plays roles in cell migration and angiogenesis. CYLD is involved in other physiological processes, such as immune response, inflammation, cell cycle progression, spermatogenesis and osteoclastogenesis. CYLD is mutated at low frequencies in various tumors. Around 25% of CYLD alterations are truncating mutations. Germline mutations in CYLD gene have been associated with cylindromatosis, multiple familial trichoepithelioma, and Brooke-Spiegler syndrome.

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