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Recent advancements in gene editing using the CRISPR-Cas9 system and a report implying activity of the AID system in P. falciparum (Ghorbal et al., 2014; Kreidenweiss et al., 2013; Wagner et al., 2014) should permit application of the degradation technology to effectively examine endogenous protein function in the human malaria parasite.
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A piggyBac transposon-based enhancer-trap system was developed that functions efficiently in the human malaria vector, Anopheles stephensi.
The varieties of gene amplification, diversification and hypervariability in the human malaria parasite, Plasmodium falciparum.
Windbichler, N. et al. A synthetic homing endonuclease-based gene drive system in the human malaria mosquito.
Ghorbal, M. et al. Genome editing in the human malaria parasite Plasmodium falciparum using the CRISPR-Cas9 system.
In the human malaria parasites Plasmodium falciparum, histone modifications have been implicated in the transcriptional regulation.
Drug resistances in the human malaria parasite, P. falciparum, were also observed in vitro [3].
In the human malaria parasite Plasmodium falciparum, the single PDC is located exclusively in the apicoplast.
Effector proteins that initiate the autophagy pathway in the human malaria parasite remain unknown.
Furthermore, wAlbB conferred resistance in the mosquito to the human malaria parasite Plasmodium falciparum.
Close relatives of the human malaria parasites remain common in chimpanzees.
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