ArticleBiology open2015
Hemoglobin S and C affect protein export in Plasmodium falciparum-infected erythrocytes.
Article in Biology open, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Beyond Iron Deficiency: An Atypical Peripheral Smear Revealing Hemoglobin C in an Adolescent.Cureus · 2026Article
- Phenotypic screens reveal Plasmodium falciparum genetic factors associated with infection of sickle-trait cells.Blood cells, molecules & diseases · 2025Article
- Natural Acquired Immunity to Malaria Antigens among Pregnant Women with Hemoglobin C Trait.The American journal of tropical medicine and hygiene · 2022Article
- PfEMP1-Specific Immunoglobulin G Reactivity Among Beninese Pregnant Women With Sickle Cell Trait.Open forum infectious diseases · 2021Article
- Decreased parasite burden and altered host response in children with sickle cell anemia and severe anemia with malaria.Blood advances · 2021Article
- Impact of Sickle Cell Trait Hemoglobin on the Intraerythrocytic Transcriptional Program of Plasmodium falciparum.mSphere · 2021Article
- Functionalized supported membranes for quantifying adhesion of P. falciparum-infected erythrocytes.Biophysical journal · 2021Article
- Chemical Biology Tools To Investigate Malaria Parasites.Chembiochem : a European journal of chemical biology · 2021Review
- Host Cytoskeleton Remodeling throughout the Blood Stages of Plasmodium falciparum.Microbiology and molecular biology reviews : MMBR · 2019Review
- Born to sweet delight: Using natural models of malaria protection to understand and neutralize P. falciparum pathogenesis.PLoS pathogens · 2019Article
- Impact of Hemoglobin S Trait on Cell Surface Antibody Recognition ofOpen forum infectious diseases · 2019Article
- Hemoglobin S and C affect biomechanical membrane properties ofCommunications biology · 2019Article
- Hemoglobin E, malaria and natural selection.Evolution, medicine, and public health · 2019Review
- Role of phospholipid synthesis in the development and differentiation of malaria parasites in the blood.The Journal of biological chemistry · 2018Review
- The role of the red blood cell in host defence against falciparum malaria: an expanding repertoire of evolutionary alterations.British journal of haematology · 2017Review
- Hemoglobin variants shape the distribution of malaria parasites in human populations and their transmission potential.Scientific reports · 2017Article
- Ankyrin-1 Gene Exhibits Allelic Heterogeneity in Conferring Protection Against Malaria.G3 (Bethesda, Md.) · 2017Article
- Rolling Adhesion of Schizont Stage Malaria-Infected Red Blood Cells in Shear Flow.Biophysical journal · 2017Article
- Heterozygous HbAC but not HbAS is associated with higher newborn birthweight among women with pregnancy-associated malaria.Scientific reports · 2017Article
- Differential time-dependent volumetric and surface area changes and delayed induction of new permeation pathways in P. falciparum-infected hemoglobinopathic erythrocytes.Cellular microbiology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malaria is a potentially deadly disease. However, not every infected person develops severe symptoms. Some people are protected by naturally occurring mechanisms that frequently involve inheritable modifications in their hemoglobin. The best studied protective hemoglobins are the sickle cell hemoglobin (HbS) and hemoglobin C (HbC) which both result from a single amino acid substitution in β-globin: glutamic acid at position 6 is replaced by valine or lysine, respectively. How these hemoglobinopathies protect from severe malaria is only partly understood. Models currently proposed in the literature include reduced disease-mediating cytoadherence of parasitized hemoglobinopathic erythrocytes, impaired intraerythrocytic development of the parasite, dampened inflammatory responses, or a combination thereof. Using a conditional protein export system and tightly synchronized Plasmodium falciparum cultures, we now show that export of parasite-encoded proteins across the parasitophorous vacuolar membrane is delayed, slower, and reduced in amount in hemoglobinopathic erythrocytes as compared to parasitized wild type red blood cells. Impaired protein export affects proteins targeted to the host cell cytoplasm, Maurer's clefts, and the host cell plasma membrane. Impaired protein export into the host cell compartment provides a mechanistic explanation for the reduced cytoadherence phenotype associated with parasitized hemoglobinopathic erythrocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.