Abhisheka Bansal

TL;DR: It is shown that knocking out the P. falciparum variant-silencing SET gene (here termed PfSETvs), which encodes an orthologue of Drosophila melanogaster ASH1 and controls histone H3 lysine 36 trimethylation (H3K36me3) on var genes, results in the transcription of virtually all var genes in the single parasite nuclei and their expression as proteins on the surface of individual infected red blood cells.

TL;DR: In this article, a peptide P3 from the junction domain of Plasmodium falciparum CDPK1 (PfCDPK) as well as purfalcamine inhibit functional activity to block microneme discharge and erythrocyte invasion.

TL;DR: It is shown that the malaria parasite can rapidly evolve to adapt for loss of an “essential” kinase, PfCDPK1, and C DPK1 was successfully disrupted in the mutant parasites using CRISPR/Cas9 and conclusively demonstrates that CDPK 1 is a good target for developing transmission-blocking drugs.

TL;DR: The successful knockout of PfCDPK2 from blood-stage parasites, which was previously thought to be indispensable for parasite growth in red blood cells, is demonstrated and suggests that targeting PfC DPK2 may be a good strategy to control malaria transmission in countries with high transmission.

TL;DR: Replacement of the wild-type threonine gatekeeper residue with methionine reduces the transphosphorylation activity of CDPK1, suggesting that targeting two kinases may be more effective in chemotherapy to treat malaria so as not to select for mutations in one of the enzymes.