MALARIAL ADENOSINE DEAMINASES

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 恶性疟原虫是嘌呤营养缺陷型，从红细胞中回收嘌呤用于合成RNA和DNA。次黄嘌呤是疟原虫嘌呤代谢的关键前体。腺苷脱氨酶是从腺苷中回收次黄嘌呤的关键酶之一，共甲霉素衍生物是一类很有前途的有效天然产物过渡态类似物疟疾腺苷脱氨酶抑制剂。识别甲硫基腺苷底物疟疾，但不是人类，腺苷脱氨酶的基础选择性抑制甲硫基coformycin。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Plasmodium falciparum is a purine auxotroph, salvaging purines from erythrocytes for synthesis of RNA and DNA. Hypoxanthine is the key precursor for purine metabolism in Plasmodium. Adenosine deaminase is one of key enzymes to salvage hypoxanthine from adenosine in this parasite and the coformycin-derivates represent a promising class of potent natural-product transition state analogue inhibitors of malarial adenosine deaminase. Recognition of a methylthio-adenosine substrate by malarial, but not human, adenosine deaminase underlies selective inhibition by methylthio-coformycin.