ArticleCell host & microbe2013
A host GPCR signaling network required for the cytolysis of infected cells facilitates release of apicomplexan parasites.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 42 citations in OpenAlex.
- An in vivo fitness gene of Toxoplasma, MIC11, is essential for PLP1-mediated egress from host cells.Nature communications · 2026Article
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- Inhibition of malaria and babesiosis parasites by putative red blood cell targeting small molecules.Frontiers in cellular and infection microbiology · 2024Article
- iTRAQ-Based Phosphoproteomic Analysis Exposes Molecular Changes in the Small Intestinal Epithelia of Cats afterAnimals : an open access journal from MDPI · 2023Article
- Role of Host Small GTPases in Apicomplexan Parasite Infection.Microorganisms · 2022Review
- Malaria parasite egress at a glance.Journal of cell science · 2021Review
- Insilico Functional Analysis of Genome-Wide Dataset From 17,000 Individuals Identifies Candidate Malaria Resistance Genes Enriched in Malaria Pathogenic Pathways.Frontiers in genetics · 2021Article
- CRISPR/Cas9-Based Knockout of GNAQ Reveals Differences in Host Cell Signaling Necessary for Egress of Apicomplexan Parasites.mSphere · 2020Article
- Analysis of erythrocyte signalling pathways during Plasmodium falciparum infection identifies targets for host-directed antimalarial intervention.Nature communications · 2020Article
- An exported kinase family mediates species-specific erythrocyte remodelling and virulence in human malaria.Nature microbiology · 2020Article
- Toxoplasma gondii induces prolonged host epidermal growth factor receptor signalling to prevent parasite elimination by autophagy: Perspectives for in vivo control of the parasite.Cellular microbiology · 2019Article
- Phosphatidic acid governs natural egress in Toxoplasma gondii via a guanylate cyclase receptor platform.Nature microbiology · 2019Article
- Druggable Targets in Cyclic Nucleotide Signaling Pathways in Apicomplexan Parasites and Kinetoplastids against Disabling Protozoan Diseases in Humans.International journal of molecular sciences · 2019Review
- Sequential Membrane Rupture and Vesiculation during Plasmodium berghei Gametocyte Egress from the Red Blood Cell.Scientific reports · 2018Article
- Red blood cells release microparticles containing human argonaute 2 and miRNAs to target genes of Plasmodium falciparum.Emerging microbes & infections · 2017Article
- Article
- Toxoplasma gondii GRA7-Targeted ASC and PLD1 Promote Antibacterial Host Defense via PKCα.PLoS pathogens · 2017Article
- Potential Sabotage of Host Cell Physiology by Apicomplexan Parasites for Their Survival Benefits.Frontiers in immunology · 2017Review
- Expanding the antimalarial toolkit: Targeting host-parasite interactions.The Journal of experimental medicine · 2016Review
- Host-pathogen interactions in malaria: cross-kingdom signaling and mitochondrial regulation.Current opinion in immunology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Following intracellular replication, the apicomplexan parasites Plasmodium falciparum and Toxoplasma gondii cause host cell cytolysis to facilitate parasite release and disease progression. Parasite exit from infected cells requires the interplay of parasite-derived proteins and host actin cytoskeletal changes; however, the host proteins underlying these changes remain obscure. We report the identification of a Gα(q)-coupled host-signaling cascade required for the egress of both P. falciparum and T. gondii. Gα(q)-coupled signaling results in protein kinase C (PKC)-mediated loss of the host cytoskeletal protein adducin and weakening of the cellular cytoskeleton. This cytoskeletal compromise induces catastrophic Ca(2+) influx mediated by the mechanosensitive cation channel TRPC6, which activates host calpain that proteolyzes the host cytoskeleton allowing parasite release. Reinforcing the feasibility of targeting host proteins as an antiparasitic strategy, mammalian PKC inhibitors demonstrated activity in murine models of malaria and toxoplasmosis. Importantly, an orally bioavailable PKC inhibitor prolonged survival in an experimental cerebral malaria model.
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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.