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首页> 外文期刊>Expert opinion on therapeutic targets >Misrouted cell surface receptors as a novel disease aetiology and potential therapeutic target: the case of hypogonadotropic hypogonadism due to gonadotropin-releasing hormone resistance.
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Misrouted cell surface receptors as a novel disease aetiology and potential therapeutic target: the case of hypogonadotropic hypogonadism due to gonadotropin-releasing hormone resistance.

机译：误导的细胞表面受体作为一种新型疾病病因和潜在的治疗靶点：由于促性腺激素释放激素抵抗而导致的促性腺激素性性腺功能减退症。

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摘要

Molecules that are incorrectly folded or defectively assembled are recognised by cellular quality control mechanisms. This leads such conformationally abnormal molecules to intracellular retention and eventual degradation. A number of diseases caused by mutations that interfere with proper processing and intracellular trafficking of key cell surface proteins have been described. These include a particular variant of hypogonadotropic hypogonadism, which results from mislocalisation of the gonadotropin-releasing hormone (GnRH) receptor. It has been shown recently that membrane expression and function of misfolded GnRH receptor mutants can be rescued by a peptidomimetic antagonist of GnRH (IN3) that permeates into the cell and reaches the abnormally manufactured nascent receptor, stabilising a conformation compatible with cell-surface transport and reversing intracellular retention. This approach seems applicable for the development of defined therapeutic strategies for an array of diseases caused by incorrectly routed cell surface or secreted proteins.
机译：细胞质量控制机制可以识别折叠不正确或组装不正确的分子。这导致这种构象异常分子导致细胞内滞留并最终降解。已经描述了由突变引起的许多疾病，这些疾病干扰关键细胞表面蛋白的正常加工和细胞内运输。这些包括促性腺激素减退性腺功能减退症的特定变体，这是由于促性腺激素释放激素（GnRH）受体的定位错误而引起的。最近显示，可以通过渗透到细胞中并到达异常制造的新生受体的GnRH的拟肽拮抗剂（IN3）来挽救错误折叠的GnRH受体突变体的膜表达和功能，从而稳定与细胞表面转运和逆转细胞内滞留。这种方法似乎可用于开发针对由路线不正确的细胞表面或分泌的蛋白质引起的一系列疾病的明确治疗策略。

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