Gliding motility and host cell invasion by the apicomplexan parasite Plasmodium falciparum (Pf), the causative agent of malaria, is powered by a macromolecular complex called the glideosome that lies between the parasite plasma membrane and the inner membrane complex.
Plasmodium species cause malaria by proliferating in human erythrocytes.
The assay uses magnetic beads conjugated with anti-HRP2 antibody for protein capture and concentration, and antibody-conjugated quantum dots for optical detection. Western blot analysis demonstrated that magnetic beads allow the concentration of HRP2 protein in urine by 20-fold.
We show that two P. knowlesi invasion ligands, PkDBPβ and PkDBPγ, bind specifically to Neu5Gc-containing receptors. A human-adapted P. knowlesi line invades human RBCs independently of Neu5Gc, with duplication of the sialic acid-independent invasion ligand, PkDBPα and loss of PkDBPγ.
This study was conducted to determine the malaria parasite density among children using actual white blood cell (WBC) and the assumed WBC counts (8.0 × 109/l).
This detailed analysis of TSS usage enabled us to define architectural features of plasmodial promoters. We demonstrate that TSS selection and strength are constrained by local nucleotide composition.
In this study, we show that the human malaria parasite Plasmodium falciparum expresses at its surface a member of the microbial formate–nitrite transporter family (PfFNT), which, when expressed in Xenopus laevis oocytes, transports both formate and lactate.
The results revealed a significant difference in the age distribution of clinical cases between passive and active case surveillance, and between clinical case rate and asymptomatic parasite rate.
We have produced RNA-seq data and utilised it to improve gene-model prediction and to provide quantitative, genome-wide, data on gene expression. Comparison of the RMP genomes with the genome of the human malaria parasite P. falciparum and RNA-seq mapping permitted gene annotation at base-pair resolution.
This study provides evidence that susceptibility to malaria parasite infection increases during pregnancy, and, as shown before, in younger individuals, which points towards similar dynamics of malaria parasite infection in human and chimpanzee populations and raises questions about the effects of such infections on pregnancy outcome and offspring morbidity/mortality.
