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首页> 外文会议>American Peptide Symposium >Inhibition of pathogenically-related morphologic transition in Candida albicans by disrupting Cdc42 binding to its effectors
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Inhibition of pathogenically-related morphologic transition in Candida albicans by disrupting Cdc42 binding to its effectors

机译：通过破坏CDC42结合其效应抑制念珠菌与念珠菌的致病性形态转变

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Signal transduction pathways are typically regulated by protein-protein interaction networks. As many human diseases exhibit dysfunctional aspects in these networks, there has been a great deal of enthusiasm for the prospect of identifying novel drug candidates targeting key signal transduction components in human diseases. Candida albicans is an opportunistic fungal pathogen that is the cause of most "yeast infections" or candidiasis in humans. The pathogenicity of C. albicans is contingent upon its ability to switch from yeast to hyphal growth in response to environmental signals. Invasive hyphal growth requires signal transduction through the interaction of Candida Cdc42 (CaCdc42), a small GTPase of the Rho-family, with the CRIB (Cdc42/Rac Interactive Binding) domains of its two downstream effectors, Cst20 and CaCla4, under all conditions examined [1]. Thus, these protein-protein interactions are potential targets for curbing candidiasis and that the CRIB peptides may function as potent anti-fungal agents against the CaCdc42. In this work, we have investigated the intracellular activities of the CRIB peptides transduced by a peptide transduction domain (i.e. NPF: VLTNENPFSDP [2]), in inhibiting the morphologic transition of C. albicans.
机译：信号转导途径通常由蛋白质 - 蛋白质相互作用网络调节。由于许多人类疾病在这些网络中表现出存在功能失调的方面，对鉴定人类疾病的关键信号转导组分鉴定新型药物候选者的前景，这是一个很大的热情。念珠菌白醛人是一种机会主义的真菌病原体，是大多数“酵母感染”或人类念珠菌病的原因。 C. albicans的致病性对其在响应环境信号响应于酵母切换到亚酚醛生长的能力。侵袭性亚酚醛生长需要通过Candida CDC42（CaCDC42）的相互作用，rho家族的小GTP酶的相互作用，其两个下游效应器，CST20和CaClA4的婴儿床（CDC42 / RAC互动结合）结构域在所有条件下检查[1]。因此，这些蛋白质 - 蛋白质相互作用是用于抑制念珠菌病的潜在靶标，并且婴儿床肽可以用作符合CACDC42的有效的抗真菌剂。在这项工作中，我们研究了通过肽转导结构域转导的婴儿床肽的细胞内活性（即NPF：VLTNENPFSDP [2]），抑制C. albicans的形态转变。

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