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Heterochromatin Silencing and Locus Repositioning Linked to Regulation of Virulence Genes in Plasmodium falciparum
TLDR
It is demonstrated that both a subtelomeric transgene and var genes are subject to reversible gene silencing, which implies that locus repositioning and heterochromatic silencing play important roles in the epigenetic regulation of virulence genes in P. falciparum. Expand
Molecular Mechanism for Switching of P. falciparum Invasion Pathways into Human Erythrocytes
TLDR
It is shown that switching from sialic acid–dependent to –independent invasion is reversible and depends on parasite ligand use, and differential activation of PfRh4 represents a previously unknown mechanism to switch invasion pathways and provides P. falciparum with exquisite adaptability in the face of erythrocyte receptor polymorphisms and host immune responses. Expand
Phenotypic variation of Plasmodium falciparum merozoite proteins directs receptor targeting for invasion of human erythrocytes
TLDR
Phenotypic variation of the PfRh protein family allows P.falciparum to exploit different patterns of receptors on the erythrocyte surface and thereby respond to polymorphisms in ery Throcyte receptors and to evade the host immune system. Expand
BASIGIN is a receptor essential for erythrocyte invasion by Plasmodium falciparum
TLDR
The discovery of a cross-strain dependency on a single extracellular receptor–ligand pair for erythrocyte invasion by P. falciparum provides a focus for new anti-malarial therapies. Expand
Plasmodium falciparum erythrocyte invasion through glycophorin C and selection for Gerbich negativity in human populations
TLDR
It is shown that the receptor for EBA140 is glycophorin C (GYPC) and that this interaction mediates a principal P. falciparum invasion pathway into human erythrocytes, providing compelling evidence that Ge negativity has arisen in Melanesian populations through natural selection by severe malaria. Expand
The tyrosine-86 allele of the pfmdr1 gene of Plasmodium falciparum is associated with increased sensitivity to the anti-malarials mefloquine and artemisinin.
TLDR
The data support a hypothesis where the pfmdr1 gene confers a true multidrug resistance phenotype which is lost by mutation, and an intragenic association was found between a polymorphism in the polyasparagine linker region of pfmDr1 and the tyr-86 allele, which may be due to genetic hitchhiking, indicative of recent selection by chloroquine. Expand
The pfmdr1 Gene Is Associated with a Multidrug-Resistant Phenotype in Plasmodium falciparumfrom the Western Border of Thailand
TLDR
The relationship between pfmdr1 and resistance to structurally distinct antimalarial agents confirms the presence of a true multidrug-resistant phenotype. Expand
A Plant-Like Kinase in Plasmodium falciparum Regulates Parasite Egress from Erythrocytes
TLDR
It is found that the plant-like calcium-dependent protein kinase PfCDPK5, which is expressed in invasive merozoite forms of Plasmodium falciparum, was critical for egress from the human host erythrocyte, an essential step in the parasite life cycle. Expand
Negative selection of Plasmodium falciparum reveals targeted gene deletion by double crossover recombination.
TLDR
The use of negative selection for gene disruptions via double crossover recombination will dramatically improve the ability to analyse protein function and opens the possibility of using this strategy for a variety of gene deletion and modification experiments in the analysis of this important infectious agent. Expand
Contribution of the pfmdr1 gene to antimalarial drug-resistance.
TLDR
Although not essential for chloroquine-resistance, pfmdr1 plays a role in modulating levels of resistance and appears to be a significant component in resistance to the structurally related drug quinine. Expand
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