Human lymphoid malignancies inherit gene expression networks from their normal B-cell counterpart and co-opt them for their own oncogenic purpose, which is usually governed by transcription factors and signaling pathways. These transcription factors and signaling pathways are precisely regulated at multiple steps, including ubiquitin modification. Protein ubiqutination plays a role in almost all cellular events and in many human diseases. In the past few years, multiple studies have expanded the role of ubiquitination in the genesis of diverse lymphoid malignancies. Here, we discuss our current understanding of both proteolytic and non-proteolytic functions of the protein ubiquitination system and describe how it is involved in the pathogenesis of human lymphoid cancers. Lymphoid-restricted ubiquitination mechanisms, including ubiquitin E3 ligases and deubiquitinating enzymes, provide great opportunities for the development of targeted therapies for lymphoid cancers.

中文翻译：

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淋巴恶性肿瘤中的蛋白质泛素化。

人类淋巴恶性肿瘤从其正常的B细胞对等体继承基因表达网络，并为自己的致癌目的而选择它们，这通常由转录因子和信号通路控制。这些转录因子和信号传导途径在包括泛素修饰在内的多个步骤中得到精确调控。蛋白质泛素化在几乎所有细胞事件和许多人类疾病中都起作用。在过去的几年中，多项研究扩大了泛素化在多种淋巴恶性肿瘤发生中的作用。在这里，我们讨论我们对蛋白质泛素化系统的蛋白水解和非蛋白水解功能的当前理解，并描述其如何参与人类淋巴癌的发病机理。淋巴限制的泛素化机制，