ArticleBlood2006
Solute transport via the new permeability pathways in Plasmodium falciparum-infected human red blood cells is not consistent with a simple single-channel model.
Article in Blood, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Multi-Omics Advancements towardsDiagnostics (Basel, Switzerland) · 2021Review
- Pan-active imidazolopiperazine antimalarials target the Plasmodium falciparum intracellular secretory pathway.Nature communications · 2020Article
- Novel Plasmodium falciparum metabolic network reconstruction identifies shifts associated with clinical antimalarial resistance.BMC genomics · 2017Article
- Uptake of purines in Plasmodium falciparum-infected human erythrocytes is mostly mediated by the human equilibrative nucleoside transporter and the human facilitative nucleobase transporter.Malaria journal · 2010Article
- Malaria parasite mutants with altered erythrocyte permeability: a new drug resistance mechanism and important molecular tool.Future microbiology · 2010Review
- Rodent and nonrodent malaria parasites differ in their phospholipid metabolic pathways.Journal of lipid research · 2010Article
- Plasmodium berghei-infection induces volume-regulated anion channel-like activity in human hepatoma cells.Cellular microbiology · 2009Article
- The Plasmodium falciparum-induced anion channel of human erythrocytes is an ATP-release pathway.Pflugers Archiv : European journal of physiology · 2009Article
- Plasmodium falciparum regulatory subunit of cAMP-dependent PKA and anion channel conductance.PLoS pathogens · 2008Article
- Electrophysiological studies of malaria parasite-infected erythrocytes: current status.International journal for parasitology · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
After infection of a red blood cell (RBC), the malaria parasite, Plasmodium falciparum, increases the permeability of the host's plasma membrane by inducing new permeability pathways (NPPs). Single-channel patch-clamp experiments have shown the presence in infected RBCs of novel anion-selective channel types with low open-state probabilities at positive membrane potentials. These channels have been postulated to form the NPPs. Here, we have used a range of transport techniques to study whether electroneutral solutes use these channels or altered/separate pathways. Transport of the electroneutral solute sorbitol via the NPPs was found to increase by a small but significant amount after gross membrane depolarization. This is inconsistent with transport via a channel with a reduced open-state probability at positive membrane potentials. As has been demonstrated previously for parasite-induced anion currents, sorbitol transport in infected RBCs was found to be sensitive to the presence of bovine serum albumin (BSA). However, it remains to be shown whether the effect is due to serum/BSA altering a single channel type or activating a new pathway. In addition, the study highlights problems that can occur when using different transport techniques to study the NPPs.
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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.