umu.sePublications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
A Stem Cell Strategy Identifies Glycophorin C as a Major Erythrocyte Receptor for the Rodent Malaria Parasite Plasmodium berghei
Show others and affiliations
2016 (English)In: PLoS ONE, E-ISSN 1932-6203, Vol. 11, no 6, article id e0158238Article in journal (Refereed) Published
Abstract [en]

The clinical complications of malaria are caused by the parasite expansion in the blood. Invasion of erythrocytes is a complex process that depends on multiple receptor-ligand interactions. Identification of host receptors is paramount for fighting the disease as it could reveal new intervention targets, but the enucleated nature of erythrocytes makes genetic approaches impossible and many receptors remain unknown. Host-parasite interactions evolve rapidly and are therefore likely to be species-specific. As a results, understanding of invasion receptors outside the major human pathogen Plasmodium falciparum is very limited. Here we use mouse embryonic stem cells (mESCs) that can be genetically engineered and differentiated into erythrocytes to identify receptors for the rodent malaria parasite Plasmodium berghei. Two proteins previously implicated in human malaria infection: glycophorin C (GYPC) and Band-3 (Slc4a1) were deleted in mESCs to generate stable cell lines, which were differentiated towards erythropoiesis. In vitro infection assays revealed that while deletion of Band-3 has no effect, absence of GYPC results in a dramatic decrease in invasion, demonstrating the crucial role of this protein for P. berghei infection. This stem cell approach offers the possibility of targeting genes that may be essential and therefore difficult to disrupt in whole organisms and has the potential to be applied to a variety of parasites in diverse host cell types.

Place, publisher, year, edition, pages
Public Library of Science , 2016. Vol. 11, no 6, article id e0158238
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:umu:diva-165845DOI: 10.1371/journal.pone.0158238ISI: 000378865200051PubMedID: 27362409OAI: oai:DiVA.org:umu-165845DiVA, id: diva2:1379084
Funder
Wellcome trustAvailable from: 2019-12-16 Created: 2019-12-16 Last updated: 2019-12-18Bibliographically approved

Open Access in DiVA

fulltext(1937 kB)14 downloads
File information
File name FULLTEXT01.pdfFile size 1937 kBChecksum SHA-512
5381cf94d0709cdbe5a62e1b87a5ec75940b2fdedcbea61ce6b0a58ac1b67e82cef3aaf222014b6e0955c754537c82c8de50c1308c2e3e784e179f7db8f607ac
Type fulltextMimetype application/pdf

Other links

Publisher's full textPubMed

Authority records BETA

Billker, Oliver

Search in DiVA

By author/editor
Billker, Oliver
In the same journal
PLoS ONE
Cell and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar
Total: 14 downloads
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

doi
pubmed
urn-nbn

Altmetric score

doi
pubmed
urn-nbn
Total: 17 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf