Abstract
The human serum protein apolipoprotein L1 (APOL1) kills Trypanosoma brucei but not the sleeping sickness agent Trypanosoma rhodesiense. APOL1 C-terminal variants can kill T. rhodesiense but they also induce kidney disease. Given topological and functional differences between intracellular and extracellular APOL1 isoforms, I propose that trypanolysis and kidney disease result from distinct APOL1 activities.
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