Taenia solium can cause human taeniasis and/or cysticercosis. The latter can in some instances cause human neurocysticercosis which is considered a priority in disease‐control strategies and the prevention of mental health problems. Glutathione transferases are crucial for the establishment and long‐term survival of T. solium; therefore, we structurally analyzed the 24‐kDa glutathione transferase gene (Ts24gst) of T. solium and biochemically characterized its product. The gene promoter showed potential binding sites for transcription factors and xenobiotic regulatory elements. The gene consists of a transcription start site, four exons split by three introns, and a polyadenylation site. The gene architecture is conserved in cestodes. Recombinant Ts24GST (rTs24GST) was active and dimeric. Anti‐rTs24GST serum showed slight cross‐reactivity with human sigma‐class GST. A 3D model of Ts24GST enabled identification of putative residues involved in interactions of the G‐site with GSH and of the H‐site with CDNB and prostaglandin D2. Furthermore, rTs24GST showed optimal activity at 45 °C and pH 9, as well as high structural stability in a wide range of temperatures and pHs. These results contribute to the better understanding of this parasite and the efforts directed to fight taeniasis/cysticercosis.

中文翻译：

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猪带绦虫 24-kDa 谷胱甘肽转移酶 sigma 的生化特征和基因结构分析

猪带绦虫可引起人类绦虫病和/或囊尾蚴病。后者在某些情况下会导致人类神经囊尾蚴病，这被认为是疾病控制策略和预防心理健康问题的优先事项。谷胱甘肽转移酶对于细胞的建立和长期生存至关重要猪绦虫;因此，我们对 24-kDa 谷胱甘肽转移酶基因进行了结构分析（TS24GST） 的猪绦虫并对其产物进行生化表征。基因启动子显示出转录因子和外源调节元件的潜在结合位点。该基因由一个转录起始位点、被三个内含子分裂的四个外显子和一个聚腺苷酸化位点组成。基因结构在绦虫中是保守的。重组 Ts24GST (rTs24GST) 具有活性且呈二聚体。抗 rTs24GST 血清与人 sigma 类 GST 表现出轻微的交叉反应。 Ts24GST 的 3D 模型能够识别参与 G 位点与 GSH 以及 H 位点与 CDNB 和前列腺素 D 相互作用的推定残基2。此外，rTs24GST 在 45 °C 和 pH 9 下表现出最佳活性，并在较宽的温度和 pH 范围内表现出高结构稳定性。这些结果有助于更好地了解这种寄生虫以及对抗绦虫病/囊尾蚴病的努力。