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• W1989282439 abstract "HAT (human African trypanosomiasis), caused by the protozoan parasite Trypanosoma brucei, is an emerging disease for which new drugs are needed. Expression of plasma membrane proteins [e.g. VSG (variant surface glycoprotein)] is crucial for the establishment and maintenance of an infection by T. brucei. Transport of a majority of proteins to the plasma membrane involves their translocation into the ER (endoplasmic reticulum). Thus inhibition of protein import into the ER of T. brucei would be a logical target for discovery of lead compounds against trypanosomes. We have developed a TbRM (T. brucei microsome) system that imports VSG_117 post-translationally. Using this system, MAL3-101, equisetin and CJ-21,058 were discovered to be small molecule inhibitors of VSG_117 translocation into the ER. These agents also killed bloodstream T. brucei in vitro; the concentrations at which 50% of parasites were killed (IC50) were 1.5 μM (MAL3-101), 3.3 μM (equisetin) and 7 μM (CJ-21,058). Thus VSG_117 import into TbRMs is a rapid and novel assay to identify ‘new chemical entities’ (e.g. MAL3-101, equisetin and CJ-21,058) for anti-trypanosome drug development." @default.
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• W1989282439 date "2009-03-27" @default.
• W1989282439 modified "2023-09-24" @default.
• W1989282439 title "Post-translational import of protein into the endoplasmic reticulum of a trypanosome: an <i>in vitro</i> system for discovery of anti-trypanosomal chemical entities" @default.
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• W1989282439 doi "https://doi.org/10.1042/bj20081787" @default.
• W1989282439 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2769561" @default.
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