<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rehn T</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>Jürgen Manchot Stiftung</funding><funding>Leibniz Center Infection</funding><pagination>1183</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9230084</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(6)</volume><pubmed_abstract>&lt;i>Plasmodium falciparum&lt;/i>-infected erythrocytes (&lt;i>Pf&lt;/i>IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via &lt;i>Pf&lt;/i>EMP1 proteins to escape elimination via the spleen. Evidence suggests that &lt;i>P. vivax&lt;/i>-infected reticulocytes (&lt;i>Pv&lt;/i>IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic &lt;i>P. falciparum&lt;/i> expressing &lt;i>vir&lt;/i> genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using &lt;i>vir&lt;/i> gene-expressing &lt;i>P. falciparum&lt;/i> transfectants. Those VIR proteins with a putative transmembrane domain were present in Maurer's clefts, and some were also present in the erythrocyte membrane. The VIR protein without a transmembrane domain</pubmed_abstract><journal>Microorganisms</journal><pubmed_title>Ectopic Expression of &lt;i>Plasmodium vivax vir&lt;/i> Genes in &lt;i>P. falciparum&lt;/i> Affects Cytoadhesion via Increased Expression of Specific &lt;i>var&lt;/i> Genes.</pubmed_title><pmcid>PMC9230084</pmcid><funding_grant_id>Jana Brehmer</funding_grant_id><funding_grant_id>Torben Rehn</funding_grant_id><funding_grant_id>BR 1744/12-1</funding_grant_id><funding_grant_id>BR1744/12-1</funding_grant_id><pubmed_authors>Rehn T</pubmed_authors><pubmed_authors>Lubiana P</pubmed_authors><pubmed_authors>Roeder T</pubmed_authors><pubmed_authors>Pansegrau E</pubmed_authors><pubmed_authors>Metwally NG</pubmed_authors><pubmed_authors>Roth LK</pubmed_authors><pubmed_authors>Brehmer J</pubmed_authors><pubmed_authors>Bruchhaus I</pubmed_authors><pubmed_authors>Nguyen THT</pubmed_authors><pubmed_authors>Schmitt M</pubmed_authors><pubmed_authors>Cadar D</pubmed_authors></additional><is_claimable>false</is_claimable><name>Ectopic Expression of &lt;i>Plasmodium vivax vir&lt;/i> Genes in &lt;i>P. falciparum&lt;/i> Affects Cytoadhesion via Increased Expression of Specific &lt;i>var&lt;/i> Genes.</name><description>&lt;i>Plasmodium falciparum&lt;/i>-infected erythrocytes (&lt;i>Pf&lt;/i>IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via &lt;i>Pf&lt;/i>EMP1 proteins to escape elimination via the spleen. Evidence suggests that &lt;i>P. vivax&lt;/i>-infected reticulocytes (&lt;i>Pv&lt;/i>IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic &lt;i>P. falciparum&lt;/i> expressing &lt;i>vir&lt;/i> genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using &lt;i>vir&lt;/i> gene-expressing &lt;i>P. falciparum&lt;/i> transfectants. Those VIR proteins with a putative transmembrane domain were present in Maurer's clefts, and some were also present in the erythrocyte membrane. The VIR protein without a transmembrane domain</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jun</publication><modification>2026-04-08T10:25:27.996Z</modification><creation>2025-02-19T02:57:08.535Z</creation></dates><accession>S-EPMC9230084</accession><cross_references><pubmed>35744701</pubmed><doi>10.3390/microorganisms10061183</doi></cross_references></HashMap>