Plasmodium falciparum glucose 6‐phosphate dehydrogenase (Pf Glc6PD), compared to other Glc6PDs has an additional 300 amino acids at the N‐terminus. They are not related to Glc6PD but are similar to a family of proteins (devb) of unknown function, some of which are encoded next to Glc6PD in certain bacteria. The human devb homologue has recently been shown to have 6‐phosphogluconolactonase (6PGL) activity. This suggests Pf Glc6PD may be a bifunctional enzyme, the evolution of which has involved the fusion of adjacent genes. Further functional analysis of Pf Glc6PD has been hampered because parts of the gene could not be cloned. We have isolated and sequenced the corresponding Plasmodium berghei gene and shown it encodes an enzyme (Pb Glc6PD) with the same structure as the P. falciparum enzyme. Pb Glc6PD is 950 amino acids long with significant sequence similarity in both the devb and Glc6PD domains with the P. falciparum enzyme. The P. berghei enzyme does not have an asparagine‐rich segment between the N and C halves and it contains an insertion at the same point in the Glc6PD region as the P. falciparum enzyme but the insertion in the P. berghei is longer (110 versus 62 amino acids) and unrelated in sequence to the P. falciparum insertion. Though expression of this enzyme in bacteria produced largely insoluble protein, conditions were found where the full‐length enzyme was produced in a soluble form which was purified via a histidine tag. We show that this enzyme has both Glc6PD and 6PGL activities. Thus the first two steps of the pentose phosphate pathway are catalysed by a single novel bifunctional enzyme in these parasites.

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E‐selectin mediates the rolling of circulating leukocytes on vascular endothelial cells. A polymorphism, in which serine is substituted for arginine at position 128 (S128R) in the EGF domain, has been associated with both early‐onset atherosclerosis and SLE. We investigated whether the substitution alters the ligand‐binding properties of E‐selectin under shear flow by studying the capacity of Chinese hamster ovary cell transfectants expressing wild type (WT) or S128R E‐selectin to support interactions of neutrophils, K562 cells or HL60 cells. We initially chose to study non‐fucosylated K562 cells. No interactions were observed on WT E‐selectin, whereas S128R supported a transient tethering interaction of K562 cells, which was resistant to digestion with either neuraminidase or O‐sialoglycoprotein endopeptidase, and, in turn, could result in firm adhesion in the presence of a β2‐integrin. HL60 cells exhibited increased rolling on S128R E‐selectin. Although neuraminidase treatment inhibited all HL60 interactions with WT E‐selectin, it unmasked transient tethers on S128R. We further observed that S128R recruited significantly more neutrophils than WT E‐selectin, without affecting neutrophil rolling velocity. This polymorphism may therefore amplify leukocyte‐endothelial cell interactions and may be a factor linking the S128R polymorphism to vascular disease.