ArticleTropical medicine and health2015
The Cytoplasmic Region of Plasmodium falciparum SURFIN4.2 Is Required for Transport from Maurer's Clefts to the Red Blood Cell Surface.
Article in Tropical medicine and health, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Structural and functional insights from detailed computational analysis ofJournal of genetics · 2026Article
- An overview of the interconnectedness of the PEXEL and non-PEXEL mediated protein export iniScience · 2025Review
- Variable Surface Antigens ofProtein and peptide letters · 2024Review
- Genetic polymorphism of the extracellular region in surface associated interspersed 1.1 gene of Plasmodium falciparum field isolates from Thailand.Malaria journal · 2021Article
- Tryptophan-rich domains of Plasmodium falciparum SURFINMalaria journal · 2017Article
- Selections, frameshift mutations, and copy number variation detected on the surfMalaria journal · 2017Article
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5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundPlasmodium, the causative agent of malaria, exports many proteins to the surface of the infected red blood cell (iRBC) in order to modify it toward a structure more suitable for parasite development and survival. One such exported protein, SURFIN4.2, from the parasite of human malignant malaria, P. falciparum, was identified in the trypsin-cleaved protein fraction from the iRBC surface, and is thereby inferred to be exposed on the iRBC surface. SURFIN4.2 also localize to Maurer's clefts-parasite-derived membranous structures established in the RBC cytoplasm and tethered to the RBC membrane-and their role in trafficking suggests that they are a pathway for SURFIN4.2 transport to the iRBC surface. It has not been determined the participation of protein domains and motifs within SURFIN4.2 in transport from Maurer's clefts to the iRBC surface; and herein we examined if the SURFIN4.2 intracellular region containing tryptophan-rich (WR) domain is required for its exposure on the iRBC surface.
resultsWe generated two transgenic parasite lines which express modified SURFIN4.2, with or without a part of the intracellular region. Both recombinant SURFIN4.2 proteins were exported to Maurer's clefts. However, only SURFIN4.2 possessing the intracellular region was efficiently cleaved by surface treatment of iRBC with proteinase K.
conclusionsThese results indicate that SURFIN4.2 is exposed on the iRBC surface and that the intracellular region containing WR domain plays a role on the transport from Maurer's clefts to the iRBC membrane.
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