Mat Martin, Antja-Voy Hartley, J. Jin, Mengyao Sun, T. Lu
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引用次数: 6
摘要
促炎转录因子核因子- κ B (NF- κ B)自30年前被发现以来,已成为炎症反应和肿瘤发展的核心参与者。一般来说,异常的NF- κ B活性在肿瘤发生和获得性化疗耐药中起关键作用。这种异常的NF- κ B活性通常涉及NF- κ B的几种翻译后修饰,包括磷酸化。在本章中,我们将特别介绍NF- κ B p65亚基的磷酸化位点及其与癌症的关系。重要的是,磷酸化是由不同的激酶催化的,使用三磷酸腺苷(ATP)作为磷供体。这些激酶在癌症中经常过度活跃,因此可能作为治疗不同癌症的潜在治疗靶点。κ B实体和血液恶性肿瘤。
The proinflammatory transcription factor nuclear factor- κ B (NF- κ B) has emerged as a central player in inflammatory responses and tumor development since its discovery three decades ago. In general, aberrant NF- κ B activity plays a critical role in tumorigenesis and acquired resistance to chemotherapy. This aberrant NF- κ B activity frequently involves several post-translational modifications of NF- κ B, including phosphorylation. In this chapter, we will specifically cover the phosphorylation sites reported on the p65 subunit of NF- κ B and their relationship to cancer. Importantly, phosphorylation is catalyzed by different kinases using adenosine triphosphate (ATP) as the phosphorus donor. These kinases are frequently hyperactive in cancers and thus may serve as potential therapeutic targets to treat different cancers. κ B solid and hematological malignancies.