期刊论文详细信息
Wellcome Open Research
Visualisation of experimentally determined and predicted protein N-glycosylation and predicted glycosylphosphatidylinositol anchor addition in Trypanosoma brucei .
article
Michele Tinti1  Michael A. J. Ferguson1 
[1] Wellcome Centre for Anti-Infectives Research ,(WCAIR), School of Life Sciences, University of Dundee
关键词: Trypanosoma brucei;    proteomics;    glycobiology;    N-glycosylation;    glycosylphosphatidylinositol;    oligosaccharyltransferase;    OST;    prediction;   
DOI  :  10.12688/wellcomeopenres.17640.1
学科分类:内科医学
来源: Wellcome
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【 摘 要 】

Background: Trypanosoma brucei is a protozoan parasite and the etiological agent of human and animal African trypanosomiasis. The organismcycles between its mammalian host and tsetse vector. The host-dwelling bloodstream form of the parasite is covered with a monolayer of variant surface glycoprotein (VSG) that enables it to escape both the innate and adaptive immune systems. Within this coat reside lower-abundance surface glycoproteins that function as receptors and/or nutrient transporters. The glycosylation of theTrypanosoma brucei surface proteome is essential to evade the immune response and is mediated by three oligosaccharyltransferase genes; two of which, TbSTT3A and TbSTT3B, are expressed in the bloodstream form of the parasite.Methods: We processed a recent dataset of our laboratory to visualise putative glycosylation sites of the Trypanosoma brucei proteome. We provided a visualisation for the predictions of glycosylation carried by TbSTT3A and TbSTT3B, and we augmented the visualisation with predictions for Glycosylphosphatidylinositol anchoring sites, domains and topology of the Trypanosoma brucei proteome.Conclusions: We created a web service to explore the glycosylation sites of the Trypanosoma brucei oligosaccharyltransferases substrates, using data described in a recent publication of our laboratory. We also made a machine learning algorithm available as a web service, described in our recent publication, to distinguish between TbSTT3A and TbSTT3B substrates.

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