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- W4293716226 endingPage "988" @default.
- W4293716226 startingPage "988" @default.
- W4293716226 abstract "Human trypanosomiasis affects nearly eight million people worldwide, causing great economic and social impact, mainly in endemic areas. T. cruzi and T. brucei are protozoan parasites that present efficient mechanisms of immune system evasion, leading to disease chronification. Currently, there is no vaccine, and chemotherapy is effective only in the absence of severe clinical manifestations. Nevertheless, resistant phenotypes to chemotherapy have been described in protozoan parasites, associated with cross-resistance to other chemically unrelated drugs. Multidrug resistance is multifactorial, involving: (i) drug entry, (ii) activation, (iii) metabolism and (iv) efflux pathways. In this context, ABC transporters, initially discovered in resistant tumor cells, have drawn attention in protozoan parasites, owing to their ability to decrease drug accumulation, thus mitigating their toxic effects. The discovery of these transporters in the Trypanosomatidae family started in the 1990s; however, few members were described and functionally characterized. This review contains a brief history of the main ABC transporters involved in resistance that propelled their investigation in Trypanosoma species, the main efflux modulators, as well as ABC genes described in T. cruzi and T. brucei according to the nomenclature HUGO. We hope to convey the importance that ABC transporters play in parasite physiology and chemotherapy resistance." @default.
- W4293716226 created "2022-08-31" @default.
- W4293716226 creator A5002987883 @default.
- W4293716226 creator A5018010148 @default.
- W4293716226 creator A5039652019 @default.
- W4293716226 creator A5045997020 @default.
- W4293716226 creator A5047829048 @default.
- W4293716226 creator A5055981133 @default.
- W4293716226 date "2022-08-30" @default.
- W4293716226 modified "2023-10-18" @default.
- W4293716226 title "The History of the ABC Proteins in Human Trypanosomiasis Pathogens" @default.
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