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D. C. Ghislaine Mayer

Researcher at Manhattan College

Publications -  17
Citations -  1047

D. C. Ghislaine Mayer is an academic researcher from Manhattan College. The author has contributed to research in topics: Plasmodium falciparum & Malaria. The author has an hindex of 9, co-authored 17 publications receiving 1008 citations. Previous affiliations of D. C. Ghislaine Mayer include National Institutes of Health & Virginia Commonwealth University.

Papers
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Journal ArticleDOI

Parasite ligand-host receptor interactions during invasion of erythrocytes by Plasmodium merozoites.

TL;DR: The current state of knowledge about the receptor-ligand interactions that mediate merozoite invasion of erythrocytes is reviewed.
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Characterization of a Plasmodium falciparum erythrocyte-binding protein paralogous to EBA-175

TL;DR: The interest in BAEBL's reduced binding to Gerbich erythrocytes derives from the high frequency of theGerbich phenotype in some regions of Papua New Guinea where P. falciparum is hyperendemic.
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Glycophorin B is the erythrocyte receptor of Plasmodium falciparum erythrocyte-binding ligand, EBL-1

TL;DR: Evidence is provided 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, and Interestingly, the Efe pygmies of the Ituri forest in the Democratic Republic of the Congo have the highest gene frequency of glycoph orin B-null in the world, raising the possibility that the DBL
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Polymorphism in a Plasmodium falciparum erythrocyte-binding ligand changes its receptor specificity.

TL;DR: The results suggest that P. falciparum has evolved multiple invasion pathways dependent on polymorphisms in the BAEBL ligand, which is similar to other parasite ligand species.
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Polymorphism in the Plasmodium falciparum erythrocyte-binding ligand JESEBL/EBA-181 alters its receptor specificity.

TL;DR: Six P. falciparum DBL ligands JESEBL and BAEBL can recognize multiple receptors on the erythrocyte surface and may have been successful in endemic areas because it has mutated the ligands of the DBL family to create multiple pathways of invasion, thus making selection of refractory ERYthrocytes unlikely.