Figure 4.

Proposed model for the action of (A) quinine and (B) imatinib in S. cerevisiae cells. These models result from the integration of chemogenomics, transcriptomics and proteomics approaches (dos Santos and Sá-Correia, 2009; dos Santos et al., 2009; dos Santos and Sá-Correia, 2011; dos Santos and Sá-Correia, unpublished results), suggesting new targets and modes of action for quinine and imatinib that possess extensive functional conservation in the organisms of interest, Plasmodium falciparum, and human cells, respectively. The most important results are the identification of PfHT1 as a potential target of quinine, as well as the vacuolar H⁺-ATPase (V-ATPase) as a target of imatinib (see Genome-wide Responses and Determinants of Resistance to Antimalarial Drugs and Genome-wide Responses and Determinants of Resistance to Anticancer Drugs).