ArticleEukaryotic cell2008
Exit from host cells by the pathogenic parasite Toxoplasma gondii does not require motility.
Article in Eukaryotic cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Kiss and spit metabolomics highlight the role of host purine metabolism during pathogen infection.mSphere · 2026Article
- The Toxoplasma secreted effector TgWIP modulates dendritic cell motility by activating host tyrosine phosphatases Shp1 and Shp2.Cellular and molecular life sciences : CMLS · 2024Article
- The Toxoplasma secreted effector TgWIP modulates dendritic cell motility by activating host tyrosine phosphatases Shp1 and Shp2.Research square · 2024Article
- Toxoplasma gondii excretion of glycolytic products is associated with acidification of the parasitophorous vacuole during parasite egress.PLoS pathogens · 2022Article
- 3D holotomographic monitoring of CaParasitology research · 2022Article
- Structural, Functional, and Metabolic Alterations in Human Cerebrovascular Endothelial Cells duringMicroorganisms · 2020Article
- CD209 C-Type Lectins Promote Host Invasion, Dissemination, and Infection ofFrontiers in immunology · 2020Article
- Overview of PoultryFrontiers in veterinary science · 2020Review
- Alarmin S100A11 initiates a chemokine response to the human pathogen Toxoplasma gondii.Nature immunology · 2019Article
- Seroprevalence, risk factors and impact ofAAS open research · 2019Article
- Article
- Molecular Signaling Involved in Entry and Exit of Malaria Parasites from Host Erythrocytes.Cold Spring Harbor perspectives in medicine · 2017Review
- The IL-12 Response of Primary Human Dendritic Cells and Monocytes to Toxoplasma gondii Is Stimulated by Phagocytosis of Live Parasites Rather Than Host Cell Invasion.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- The Apicomplexan CDC/MACPF-like pore-forming proteins.Current opinion in microbiology · 2015Review
- Pyrimidinergic Receptor Activation Controls Toxoplasma gondii Infection in Macrophages.PloS one · 2015Article
- The calcium-dependent protein kinase 3 of toxoplasma influences basal calcium levels and functions beyond egress as revealed by quantitative phosphoproteome analysis.PLoS pathogens · 2014Article
- Recent insights into apicomplexan parasite egress provide new views to a kill.Current opinion in microbiology · 2013Review
- Human innate immunity to Toxoplasma gondii is mediated by host caspase-1 and ASC and parasite GRA15.mBio · 2013Article
- Prison break: pathogens' strategies to egress from host cells.Microbiology and molecular biology reviews : MMBR · 2012Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The process by which the intracellular parasite Toxoplasma gondii exits its host cell is central to its propagation and pathogenesis. Experimental induction of motility in intracellular parasites results in parasite egress, leading to the hypothesis that egress depends on the parasite's actin-dependent motility. Using a novel assay to monitor egress without experimental induction, we have established that inhibiting parasite motility does not block this process, although treatment with actin-disrupting drugs does delay egress. However, using an irreversible actin inhibitor, we show that this delay is due to the disruption of host cell actin alone, apparently resulting from the consequent loss of membrane tension. Accordingly, by manipulating osmotic pressure, we show that parasite egress is delayed by releasing membrane tension and promoted by increasing it. Therefore, without artificial induction, egress does not depend on parasite motility and can proceed by mechanical rupture of the host membrane.
Indexed as
Identifiers
What OpenQuestion holds
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.