{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Paing MM"],"funding":["National Institute of Allergy and Infectious Diseases","NIAID NIH HHS","Burroughs Wellcome Fund","NIAMS NIH HHS","Wellcome Trust"],"pagination":["e43224"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6305201"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7"],"pubmed_abstract":["Erythrocyte Binding Antigen of 175 kDa (EBA-175) has a well-defined role in binding to glycophorin A (GpA) during <i>Plasmodium falciparum</i> invasion of erythrocytes. However, EBA-175 is shed post invasion and a role for this shed protein has not been defined. We show that EBA-175 shed from parasites promotes clustering of RBCs, and EBA-175-dependent clusters occur in parasite culture. Region II of EBA-175 is sufficient for clustering RBCs in a GpA-dependent manner. These clusters are capable of forming under physiological flow conditions and across a range of concentrations. EBA-175-dependent RBC clustering provides daughter merozoites ready access to uninfected RBCs enhancing parasite growth. Clustering provides a general method to protect the invasion machinery from immune recognition"],"journal":["eLife"],"pubmed_title":["Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion."],"pmcid":["PMC6305201"],"funding_grant_id":["R01 AI080792","Extramural Research Program AI080792","R01 AI137162","P30 AR048335","097945/B/11/Z","Intramural Research Program","R56 AI080792"],"pubmed_authors":["Jensen AT","Goldberg DE","Oksman A","Tolia NH","Salinas ND","Paing MM","Adams Y"],"additional_accession":[]},"is_claimable":false,"name":"Shed EBA-175 mediates red blood cell clustering that enhances malaria parasite growth and enables immune evasion.","description":"Erythrocyte Binding Antigen of 175 kDa (EBA-175) has a well-defined role in binding to glycophorin A (GpA) during <i>Plasmodium falciparum</i> invasion of erythrocytes. However, EBA-175 is shed post invasion and a role for this shed protein has not been defined. We show that EBA-175 shed from parasites promotes clustering of RBCs, and EBA-175-dependent clusters occur in parasite culture. Region II of EBA-175 is sufficient for clustering RBCs in a GpA-dependent manner. These clusters are capable of forming under physiological flow conditions and across a range of concentrations. EBA-175-dependent RBC clustering provides daughter merozoites ready access to uninfected RBCs enhancing parasite growth. Clustering provides a general method to protect the invasion machinery from immune recognition","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Dec","modification":"2026-05-06T01:02:25.39Z","creation":"2019-03-27T00:14:35Z"},"accession":"S-EPMC6305201","cross_references":{"pubmed":["30556808"],"doi":["10.7554/eLife.43224"]}}