Ferrets exclusively synthesize Neu5Ac and express naturally humanized influenza A virus receptors.

Mammals express the sialic acids N-acetylneuraminic acid (Neu5Ac) and N-glycolylneuraminic acid (Neu5Gc) on cell surfaces, where they act as receptors for pathogens, including influenza A virus (IAV). Neu5Gc is synthesized from Neu5Ac by the enzyme cytidine monophosphate-N-acetylneuraminic acid hydroxylase (CMAH). In humans, this enzyme is inactive and only Neu5Ac is produced.

In silico QTL mapping of basal liver iron levels in inbred mouse strains.

Both iron deficiency and iron excess are detrimental in many organisms, and previous studies in both mice and humans suggest that genetic variation may influence iron status in mammals. However, these genetic factors are not well defined. To address this issue, we measured basal liver iron levels in 18 inbred strains of mice of both sexes on a defined iron diet and found ∼4-fold variation in liver iron in males (lowest 153 μg/g, highest 661 μg/g) and ∼3-fold variation in females (lowest 222 μg/g, highest 658 μg/g).

Targeting of the ring exported protein 1 to the Maurer's clefts is mediated by a two-phase process.

Early development of Plasmodium falciparum within the erythrocyte is characterized by the large-scale export of proteins to the host cell. In many cases, export is mediated by a short sequence called the Plasmodium export element (PEXEL) or vacuolar transport signal; however, a number of previously characterized exported proteins do not contain such an element. In this study, we investigated the mechanisms of export of the PEXEL-negative ring exported protein 1 (REX1).

Selective permeabilization of the host cell membrane of Plasmodium falciparum-infected red blood cells with streptolysin O and equinatoxin II.

Plasmodium falciparum develops within the mature RBCs (red blood cells) of its human host in a PV (parasitophorous vacuole) that separates the host cell cytoplasm from the parasite surface. The pore-forming toxin, SLO (streptolysin O), binds to cholesterol-containing membranes and can be used to selectively permeabilize the host cell membrane while leaving the PV membrane intact. We found that in mixtures of infected and uninfected RBCs, SLO preferentially lyses uninfected RBCs rather than infected RBCs, presumably because of differences in cholesterol content of the limiting membrane.

A cluster of ring stage-specific genes linked to a locus implicated in cytoadherence in Plasmodium falciparum codes for PEXEL-negative and PEXEL-positive proteins exported into the host cell.

Blood stages of Plasmodium falciparum export proteins into their erythrocyte host, thereby inducing extensive host cell modifications that become apparent after the first half of the asexual development cycle (ring stage). This is responsible for a major part of parasite virulence. Export of many parasite proteins depends on a sequence motif termed Plasmodium export element (PEXEL) or vacuolar transport signal (VTS).

Implication of a Plasmodium falciparum gene in the switch between asexual reproduction and gametocytogenesis.

Gametocytogenesis is fundamental for transmission of the malaria parasite Plasmodium falciparum from the human host to the mosquito vector, yet very little is understood about what triggers the switch between asexual reproduction and gametocytogenesis. Arresting the progression through the sexual cycle would block transmission of this disease. Here we identify a novel gene in P.

A novel Plasmodium falciparum ring stage protein, REX, is located in Maurer's clefts.

The asexual stages of the malaria parasite Plasmodium falciparum develop inside erythrocytes of the human host. Erythrocytes are highly specialized cells lacking organelles and trafficking machinery. The parasite must therefore establish its own transport system to export proteins and waste and import nutrients.

CLAG 9 is located in the rhoptries of Plasmodium falciparum.

Clag 9, a gene located on chromosome 9 of Plasmodium falciparum has previously been associated with the cytoadherence of parasitized erythrocytes to CD36. This gene is part of a multi-gene family found in all Plasmodium species studied to date. Using data from the Malaria Genome Sequencing Project, peptides specific for clag 9 were designed, synthesized and used to immunize mice.

Comparison of Plasmodium falciparum transfection methods.

The development of an electroporation based transfection method for Plasmodium falciparum has been very successful for the study of some genes but its efficiency remains very low. While alternative approaches have been documented, electroporation of infected red blood cells generally remains the method of choice for introducing DNA into P. falciparum.