Critical roles of glycosylphosphatidylinositol for Trypanosoma brucei
Proceedings of the National Academy of Sciences of the United States of America, ISSN: 0027-8424, Vol: 97, Issue: 19, Page: 10336-10341
2000
- 156Citations
- 90Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations156
- Citation Indexes156
- 156
- CrossRef144
- Captures90
- Readers90
- 90
Article Description
Trypanosoma brucei, the protozoan parasite responsible for sleeping sickness, evades the immune response of mammalian hosts and digestion in the gut of the insect vector by means of its coat proteins tethered to the cell surface via glycosylphosphatidylinositol (GPI) anchors. To evaluate the importance of GPI for parasite survival, we cloned and disrupted a trypanosomal gene, TbGPI10, involved in biosynthesis of GPI. TbGPI10 encodes a protein of 558 amino acids having 25% and 23% sequence identity to human PIG-B and Saccharomyces cerevisiae Gpi10p, respectively. TbGPI10 restored biosynthesis of GPI in a mouse mutant cell line defective in mouse Pig-b gene. TbGPI10 also rescued the inviability of GPI10-disrupted S. cerevisiae, indicating that TbGPI10 is the orthologue of PIG-B/GPI10 that is involved in the transfer of the third mannose to GPI. The bloodstream form of T. brucei could not lose TbGPI10; therefore, GPI synthesis is essential for growth of mammalian stage parasites. Procyclic form cells (insect stage parasites) lacking the surface coat proteins because of disruption of TbGPI10 are viable and grow slower than normal, provided that they are cultured in nonadherent flasks. In regular flasks, they adhered to the plastic surface and died. Infectivity to tsetse flies is partially impaired, particularly in the early stage. Therefore, parasite-specific inhibition of GPI biosynthesis should be an effective chemotherapy target against African trypanosomiasis.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=12944309894&origin=inward; http://dx.doi.org/10.1073/pnas.180230697; http://www.ncbi.nlm.nih.gov/pubmed/10954751; https://pnas.org/doi/full/10.1073/pnas.180230697; https://dx.doi.org/10.1073/pnas.180230697; https://www.pnas.org/content/97/19/10336
Proceedings of the National Academy of Sciences
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