UNC-51-like Kinase 1: From an Autophagic Initiator to Multifunctional Drug Target
UNC-51-like Kinase 1: From an Autophagic Initiator to Multifunctional Drug Target
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UNC-51 样激酶 1：从自噬引发剂到多功能药物靶点
DOI：
10.1021/acs.jmedchem.7b01684
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发表时间：
2018
影响因子：
7.3
通讯作者：
Liu Bo
中科院分区：
文献类型：
--
作者：
Zhang Lan;Ouyang Liang;Guo Yongzhi;Zhang Jin;Liu Bo
UNC-51 样激酶 1 (ULK1) 被称为酵母 Atgl 的直系同源物，是丝氨酸苏氨酸激酶和哺乳动物中的自噬启动子。最近，越来越多的证据揭示了 ULK1 的激酶结构域结构及其翻译后修饰，并进一步阐明了其调节自噬途径以及与多种人类疾病的关联。有趣的是，最近报道了一系列小分子靶向 ULK1 或 ULK1 调节自噬，这可能为利用它们作为新型候选药物提供线索。总而言之，这篇综述讨论了 ULK1 如何作为自噬启动子来调节其复杂的机制，以及 ULK1 如何成为潜在治疗应用的多功能靶点。
UNC-51-like kinase 1 (ULK1), known as an ortholog of the yeast Atgl, is the serine threonine kinase and the autophagic initiator in mammals. Accumulating evidence has recently revealed the kinase domain structure of ULK1 and its post-translational modifications, as well as further elucidated its regulatory autophagic pathways and associations with diverse human diseases. Interestingly, a series of small molecules have been recently reported to target ULK1 or ULK1-modulating autophagy, which may provide a clue on exploiting them as novel candidate drugs. Taken together, this review discusses how ULK1 acts as an autophagic initiator for modulation of its intricate mechanisms, as well as how ULK1 becomes a multifunctional target for potential therapeutic applications.