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dc.contributor.authorBirch, Christina M.
dc.contributor.authorHou, Han Wei
dc.contributor.authorHan, Jongyoon
dc.contributor.authorNiles, Jacquin
dc.date.accessioned2015-12-15T18:06:35Z
dc.date.available2015-12-15T18:06:35Z
dc.date.issued2015-07
dc.date.submitted2015-02
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/1721.1/100270
dc.description.abstractPlasmodium falciparum malaria parasites invade and remodel human red blood cells (RBCs) by trafficking parasite-synthesized proteins to the RBC surface. While these proteins mediate interactions with host cells that contribute to disease pathogenesis, the infected RBC surface proteome remains poorly characterized. Here we use a novel strategy (I-SELEX) to discover high affinity aptamers that selectively recognize distinct epitopes uniquely present on parasite-infected RBCs. Based on inertial focusing in spiral microfluidic channels, I-SELEX enables stringent partitioning of cells (efficiency ≥ 10[superscript 6]) from unbound oligonucleotides at high volume throughput (~2 × 10[superscript 6] cells min[superscript −1]). Using an RBC model displaying a single, non-native antigen and live malaria parasite-infected RBCs as targets, we establish suitability of this strategy for de novo aptamer selections. We demonstrate recovery of a diverse set of aptamers that recognize distinct, surface-displayed epitopes on parasite-infected RBCs with nanomolar affinity, including an aptamer against the protein responsible for placental sequestration, var2CSA. These findings validate I-SELEX as a broadly applicable aptamer discovery platform that enables identification of new reagents for mapping the parasite-infected RBC surface proteome at higher molecular resolution to potentially contribute to malaria diagnostics, therapeutics and vaccine efforts.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Director's New Innovator Award 1DP2OD007124)en_US
dc.description.sponsorshipSingapore-MIT Alliance for Research and Technology. Infectious Disease Interdisciplinary Research Groupen_US
dc.description.sponsorshipWade Funden_US
dc.description.sponsorshipMIT Startup Fundsen_US
dc.description.sponsorshipSingapore-MIT Alliance for Research and Technology. BioSystems and Micromechanics Interdisciplinary Research Groupen_US
dc.description.sponsorshipNational Science Foundation (U.S.). Graduate Research Fellowshipen_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (Chemistry/Biology Interface Training Program Grant 1-T32-GM081081)en_US
dc.language.isoen_US
dc.publisherNature Publishing Groupen_US
dc.relation.isversionofhttp://dx.doi.org/10.1038/srep11347en_US
dc.rightsCreative Commons Attribution 4.0 International Licenseen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.sourceNatureen_US
dc.titleIdentification of malaria parasite-infected red blood cell surface aptamers by inertial microfluidic SELEX (I-SELEX)en_US
dc.typeArticleen_US
dc.identifier.citationBirch, Christina M., Han Wei Hou, Jongyoon Han, and Jacquin C. Niles. “Identification of Malaria Parasite-Infected Red Blood Cell Surface Aptamers by Inertial Microfluidic SELEX (I-SELEX).” Scientific Reports 5 (July 1, 2015): 11347.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Electrical Engineering and Computer Scienceen_US
dc.contributor.mitauthorBirch, Christina M.en_US
dc.contributor.mitauthorHou, Han Weien_US
dc.contributor.mitauthorHan, Jongyoonen_US
dc.contributor.mitauthorNiles, Jacquinen_US
dc.relation.journalScientific Reportsen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsBirch, Christina M.; Hou, Han Wei; Han, Jongyoon; Niles, Jacquin C.en_US
dc.identifier.orcidhttps://orcid.org/0000-0001-7215-1439
dc.identifier.orcidhttps://orcid.org/0000-0002-6250-8796
mit.licensePUBLISHER_CCen_US
mit.metadata.statusComplete


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