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. 2020 Dec 1;3:726. doi: 10.1038/s42003-020-01454-7

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — Left: In early GIE, PfPDEδ expression is low, resulting in high cAMP levels in the parasitophorous vacuole and in the host cell, thereby activating the human PKA. PKA phosphorylates one or several proteins directly or indirectly involved in NPP activity that contributes to the uptake of drugs. Middle: In mature GIE, PfPDEδ is highly expressed and degrades cAMP, leading to a decrease in PKA phosphorylation and NPP activity. Right: In mature GIE, inhibition of PfPDEδ by tadalafil results in increased levels of cAMP that reactivate PKA and NPPs, thereby restoring uptake of drugs.