CTP biosynthesis is carried out by two pathways: salvage and de novo. CTPsyn catalyzes the latter. The study of CTPsyn activity in mammalian cells began in the 1970s, and various fascinating discoveries were made regarding the role of CTPsyn in cancer and development. However, its ability to fit into a cellular serpent-like structure, termed ‘cytoophidia,’ was only discovered a decade ago by three independent groups of scientists. Although the self-assembly of CTPsyn into a filamentous structure is evolutionarily conserved, the enzyme activity upon this self-assembly varies in different species. CTPsyn is required for cellular development and homeostasis. Changes in the expression of CTPsyn cause developmental changes in Drosophila melanogaster. A high level of CTPsyn activity and formation of cytoophidia are often observed in rapidly proliferating cells such as in stem and cancer cells. Meanwhile, the deficiency of CTPsyn causes severe immunodeficiency leading to immunocompromised diseases caused by bacteria, viruses, and parasites, making CTPsyn an attractive therapeutic target. Here, we provide an overview of the role of CTPsyn in cellular and disease perspectives along with its potential as a drug target.

CTP 生物合成通过两种途径进行：补救和从头合成。CTPsyn 催化后者。哺乳动物细胞中 CTPsyn 活性的研究始于 1970 年代，关于 CTPsyn 在癌症和发育中的作用，人们做出了各种引人入胜的发现。然而，它适应细胞蛇状结构的能力，称为“嗜细胞”，仅在十年前才被三个独立的科学家小组发现。虽然 CTPsyn 自组装成丝状结构在进化上是保守的，但这种自组装的酶活性在不同物种中有所不同。CTPsyn 是细胞发育和体内平衡所必需的。CTPsyn 表达的变化导致黑腹果蝇的发育变化. 在干细胞和癌细胞等快速增殖的细胞中经常观察到高水平的 CTPsyn 活性和嗜细胞虫的形成。同时，CTPsyn 的缺乏会导致严重的免疫缺陷，导致由细菌、病毒和寄生虫引起的免疫功能低下的疾病，使 CTPsyn 成为一个有吸引力的治疗靶点。在这里，我们概述了 CTPsyn 在细胞和疾病方面的作用及其作为药物靶标的潜力。