The Trypanosomatidae family encompasses many unicellular organisms responsible of several tropical diseases that affect humans and animals. Livestock tripanosomosis caused by Trypanosoma brucei brucei (T. brucei), Trypanosoma equiperdum (T. equiperdum) and Trypanosoma evansi (T. evansi), have a significant socio-economic impact and limit animal protein productivity throughout the intertropical zones of the world. Similarly, to all organisms, the maintenance of Ca²⁺ homeostasis is vital for these parasites, and the mechanism involved in the intracellular Ca²⁺ regulation have been widely described. However, the evidences related to the mechanisms responsible for the Ca²⁺ entry are scarce. Even more, to date the presence of a store-operated Ca²⁺ channel (SOC) has not been reported. Despite the apparent absence of Orai and STIM-like proteins in these parasites, in the present work we demonstrate the presence of a store-operated Ca²⁺-entry (SOCE) in T. equiperdum, using physiological techniques. This Ca²⁺-entry is induced by thapsigargin (TG) and 2,5-di-t-butyl-1,4-benzohydroquinone (BHQ), and inhibited by 2-aminoethoxydiphenyl borate (2APB). Additionally, the use of bioinformatics techniques allowed us to identify putative transient receptor potential (TRP) channels, present in members of the Trypanozoon family, which would be possible candidates responsible for the SOCE described in the present work in T. equiperdum.

锥虫科包括许多单细胞生物，这些生物与影响​​人类和动物的几种热带疾病有关。造成畜牧业tripanosomosis布氏锥虫布氏（布氏锥虫），锥虫疫（T.疫）和伊氏锥虫（T.伊氏），在整个世界的热带区域的显著社会经济影响和限制动物蛋白的生产力。类似地，对于所有生物来说，维持 Ca ²⁺稳态对这些寄生虫至关重要，而细胞内 Ca ²⁺的机制涉及监管已被广泛描述。然而，与负责 Ca ²⁺进入的机制相关的证据很少。更重要的是，迄今为止，还没有报道过商店经营的 Ca ²⁺通道 (SOC) 的存在。尽管明显缺乏Orai和STIM样在这些寄生虫蛋白，在本工作中，我们展示一个池操纵的Ca的存在²⁺在-entry（SOCE）T.疫，使用生理技术。这钙²⁺-进入由毒胡萝卜素 (TG) 和 2,5-二叔丁基-1,4-苯并氢醌 (BHQ) 诱导，并被 2-氨基乙氧基二苯基硼酸盐 (2APB) 抑制。此外，利用生物信息学技术，使我们能够鉴定推定瞬时受体电位（TRP）通道，目前在成员Trypanozoon家庭，这将负责SOCE可能的候选人，在目前的工作中所描述T.疫。