{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Rehn T"],"funding":["Deutsche Forschungsgemeinschaft","Jürgen Manchot Stiftung","Leibniz Center Infection"],"pagination":["1183"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9230084"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["10(6)"],"pubmed_abstract":["<i>Plasmodium falciparum</i>-infected erythrocytes (<i>Pf</i>IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via <i>Pf</i>EMP1 proteins to escape elimination via the spleen. Evidence suggests that <i>P. vivax</i>-infected reticulocytes (<i>Pv</i>IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic <i>P. falciparum</i> expressing <i>vir</i> genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using <i>vir</i> gene-expressing <i>P. falciparum</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"],"journal":["Microorganisms"],"pubmed_title":["Ectopic Expression of <i>Plasmodium vivax vir</i> Genes in <i>P. falciparum</i> Affects Cytoadhesion via Increased Expression of Specific <i>var</i> Genes."],"pmcid":["PMC9230084"],"funding_grant_id":["Jana Brehmer","Torben Rehn","BR 1744/12-1","BR1744/12-1"],"pubmed_authors":["Rehn T","Lubiana P","Roeder T","Pansegrau E","Metwally NG","Roth LK","Brehmer J","Bruchhaus I","Nguyen THT","Schmitt M","Cadar D"],"additional_accession":[]},"is_claimable":false,"name":"Ectopic Expression of <i>Plasmodium vivax vir</i> Genes in <i>P. falciparum</i> Affects Cytoadhesion via Increased Expression of Specific <i>var</i> Genes.","description":"<i>Plasmodium falciparum</i>-infected erythrocytes (<i>Pf</i>IEs) adhere to endothelial cell receptors (ECRs) of blood vessels mainly via <i>Pf</i>EMP1 proteins to escape elimination via the spleen. Evidence suggests that <i>P. vivax</i>-infected reticulocytes (<i>Pv</i>IRs) also bind to ECRs, presumably enabled by VIR proteins, as shown by inhibition experiments and studies with transgenic <i>P. falciparum</i> expressing <i>vir</i> genes. To test this hypothesis, our study investigated the involvement of VIR proteins in cytoadhesion using <i>vir</i> gene-expressing <i>P. falciparum</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","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jun","modification":"2026-04-08T10:25:27.996Z","creation":"2025-02-19T02:57:08.535Z"},"accession":"S-EPMC9230084","cross_references":{"pubmed":["35744701"],"doi":["10.3390/microorganisms10061183"]}}