Studying NPC-dependent amino acid transport, the researchers recognised that amino acid deficiency is a reason for the reduced fitness in artemisinin-resistant (ARTR) parasites. They provided evidence that upregulation of NPCs to increase amino acid acquisition is a mechanism of ARTR parasites in vitro and in human infections to compensate for fitness costs such as slower growth. The study also shows that NPCs are important for access to nutrients and drugs, and amino acid deficiency is a critical limitation in ARTR parasites.
NPCs are localised in the parasitophorous vacuolar membrane (PVM). This membrane encloses the malaria parasite in red blood cells. When the amino acid supply is reduced, such as in artemisinin-resistant parasites, the malaria parasite increases the number of nutrient permeable channels (NPCs) in the PVM. At the molecular level, the gene EXP1 plays a role in regulating the number of channels.