已证明硒蛋白I（SELENOI）是乙醇胺磷酸转移酶（EPT），其特征是非硒酶结构域，并参与内质网中磷脂酰乙醇胺（PE）的主要合成分支。因此,SELENOI缺陷可能通过PE的多种功能影响健康状态。另一方面,硒（Se）作为硒代半胱氨酸（Sec）在其肽中共价掺入SELENOI，与硒蛋白家族的其他成员一样，形成以Sec为中心的结构域。不像其他硒蛋白,含有Sec的SELENOI是在动物进化的后期形成的，在广泛的物种中，PE合成的结构域的高度保守性表明EPT活性在支持生物生存和进化中的重要性。各种因素,如物种特征(年龄和性别)，膳食营养（膳食硒和脂肪摄入量），SELENOI特异性特性（硒蛋白质组中的组织分布和等级），等。,协同调节SELENOI的表达在一个暂时不清楚的相互作用。N端和C端结构域赋予SELENOI两种不同的生化功能，即PE调节和抗氧化潜力，这可能会让它参与许多生理过程，包括神经系统疾病（尤其是遗传性痉挛性截瘫），T细胞活化,肿瘤发生，和脂肪细胞分化。在这次审查中,我们总结了SELENOI的生物学和作用的进展，通过饮食硒摄入和药物或转基因方法调节相应的病理状态，阐明了硒素表达和PE稳态的精确调节。
Selenoprotein I (SELENOI) has been demonstrated to be an ethanolamine phosphotransferase (EPT) characterized by a nonselenoenzymatic domain and to be involved in the main synthetic branch of phosphatidylethanolamine (PE) in the endoplasmic reticulum. Therefore, defects of SELENOI may affect the health status through the multiple functions of PE. On the other hand, selenium (Se) is covalently incorporated into SELENOI as selenocysteine (Sec) in its peptide, which forms a Sec-centered domain as in the other members of the selenoprotein family. Unlike other selenoproteins, Sec-containing SELENOI was formed at a later stage of animal evolution, and the high conservation of the structural domain for PE synthesis across a wide range of species suggests the importance of EPT activity in supporting the survival and evolution of organisms. A variety of factors, such as species characteristics (age and sex), diet and nutrition (dietary Se and fat intakes), SELENOI-specific properties (tissue distribution and rank in the selenoproteome), etc., synergistically regulate the expression of SELENOI in a tentatively unclear interaction. The N- and C-terminal domains confer 2 distinct biochemical functions to SELENOI, namely PE regulation and antioxidant potential, which may allow it to be involved in numerous physiological processes, including neurological diseases (especially hereditary spastic paraplegia), T cell activation, tumorigenesis, and adipocyte differentiation. In this review, we summarize advances in the biology and roles of SELENOI, shedding light on the precise regulation of SELENOI expression and PE homeostasis by dietary Se intake and pharmaceutical or transgenic approaches to modulate the corresponding pathological status.
