Genomics and Computational Biology and Department of Computer and Information Science, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
PLoS One. 2010 Jan 28;5(1):e8942. doi: 10.1371/journal.pone.0008942.
Over the course of HIV infection, virus replication is facilitated by the phosphorylation of HIV proteins by human ERK1 and ERK2 mitogen-activated protein kinases (MAPKs). MAPKs are known to phosphorylate their substrates by first binding with them at a docking site. Docking site interactions could be viable drug targets because the sequences guiding them are more specific than phosphorylation consensus sites. In this study we use multiple bioinformatics tools to discover candidate MAPK docking site motifs on HIV proteins known to be phosphorylated by MAPKs, and we discuss the possibility of targeting docking sites with drugs. Using sequence alignments of HIV proteins of different subtypes, we show that MAPK docking patterns previously described for human proteins appear on the HIV matrix, Tat, and Vif proteins in a strain dependent manner, but are absent from HIV Rev and appear on all HIV Nef strains. We revise the regular expressions of previously annotated MAPK docking patterns in order to provide a subtype independent motif that annotates all HIV proteins. One revision is based on a documented human variant of one of the substrate docking motifs, and the other reduces the number of required basic amino acids in the standard docking motifs from two to one. The proposed patterns are shown to be consistent with in silico docking between ERK1 and the HIV matrix protein. The motif usage on HIV proteins is sufficiently different from human proteins in amino acid sequence similarity to allow for HIV specific targeting using small-molecule drugs.
在 HIV 感染过程中,病毒的复制是由人类 ERK1 和 ERK2 有丝分裂原激活的蛋白激酶(MAPK)对 HIV 蛋白的磷酸化来促进的。MAPK 通过首先与它们在对接位点结合,然后磷酸化其底物。对接位点相互作用可能是可行的药物靶点,因为指导它们的序列比磷酸化共识位点更具特异性。在这项研究中,我们使用多种生物信息学工具来发现已知被 MAPK 磷酸化的 HIV 蛋白上的候选 MAPK 对接位点基序,并讨论了用药物靶向对接位点的可能性。通过对不同亚型 HIV 蛋白的序列比对,我们表明,以前在人类蛋白中描述的 MAPK 对接模式以依赖于毒株的方式出现在 HIV 基质、Tat 和 Vif 蛋白上,但不存在于 HIV Rev 蛋白上,并且出现在所有 HIV Nef 毒株上。我们修改了以前注释的 MAPK 对接模式的正则表达式,以提供一种不依赖于亚型的基序,该基序注释所有 HIV 蛋白。一个修订是基于一个已记录的人类变体的一个底物对接基序,另一个修订是将标准对接基序中所需的碱性氨基酸数量从两个减少到一个。所提出的模式与 ERK1 与 HIV 基质蛋白之间的计算机对接一致。该基序在 HIV 蛋白上的使用与人类蛋白在氨基酸序列相似性上的使用有足够的不同,允许使用小分子药物进行 HIV 特异性靶向。