@article {539686,
	title = {Glycophorin B is the erythrocyte receptor of Plasmodium falciparum erythrocyte-binding ligand, EBL-1},
	journal = {Proc Natl Acad Sci U S A},
	volume = {106},
	number = {13},
	year = {2009},
	note = {<p>Mayer, D C GhislaineCofie, JoannJiang, LubinHartl, Daniel LTracy, ErinKabat, JurajMendoza, Laurence HMiller, Louis Heng2009/03/13 09:00Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5348-52. doi: 10.1073/pnas.0900878106. Epub 2009 Mar 11.</p>},
	month = {Mar 31},
	pages = {5348-52},
	abstract = {<p>In the war against Plasmodium, humans have evolved to eliminate or modify proteins on the erythrocyte surface that serve as receptors for parasite invasion, such as the Duffy blood group, a receptor for Plasmodium vivax, and the Gerbich-negative modification of glycophorin C for Plasmodium falciparum. In turn, the parasite counters with expansion and diversification of ligand families. The high degree of polymorphism in glycophorin B found in malaria-endemic regions suggests that it also may be a receptor for Plasmodium, but, to date, none has been identified. We provide evidence from erythrocyte-binding that glycophorin B is a receptor for the P. falciparum protein EBL-1, a member of the Duffy-binding-like erythrocyte-binding protein (DBL-EBP) receptor family. The erythrocyte-binding domain, region 2 of EBL-1, expressed on CHO-K1 cells, bound glycophorin B(+) but not glycophorin B-null erythrocytes. In addition, glycophorin B(+) but not glycophorin B-null erythrocytes adsorbed native EBL-1 from the P. falciparum culture supernatants. Interestingly, the Efe pygmies of the Ituri forest in the Democratic Republic of the Congo have the highest gene frequency of glycophorin B-null in the world, raising the possibility that the DBL-EBP family may have expanded in response to the high frequency of glycophorin B-null in the population.</p>},
	keywords = {Animals, Antigens, Protozoan/*physiology, Erythrocytes/metabolism/*parasitology, Glycophorin/genetics/*metabolism, Humans, Ligands, Molecular Sequence Data, Plasmodium falciparum/*pathogenicity, Polymorphism, Genetic, Protein Binding, Protozoan Proteins/*physiology, Receptors, Cell Surface/*physiology},
	isbn = {1091-6490 (Electronic)0027-8424 (Linking)},
	author = {Mayer, D. C. and Cofie, J. and Jiang, L. and Hartl, D. L. and Tracy, E. and Kabat, J. and Mendoza, L. H. and Miller, L. H.}
}
