UNC-51-like kinase 1 (ULK1), known as an ortholog of the yeast Atg1, 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.

中文翻译：

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UNC-51样激酶1：从自噬引发剂到多功能药物靶标

UNC-51样激酶1（ULK1）被称为酵母Atg1的直系同源物，是哺乳动物中的丝氨酸-苏氨酸激酶和自噬引发剂。越来越多的证据最近揭示了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，最近已经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的候选药物提供线索。综上所述，本综述讨论了ULK1如何作为自噬引发剂来调节其复杂机制，以及ULK1如何成为潜在治疗应用的多功能靶标。