ArticlePLoS pathogens2017
Toxoplasma gondii induces FAK-Src-STAT3 signaling during infection of host cells that prevents parasite targeting by autophagy.
Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Review
- The differential roles of Giardia duodenalis-secreted tenascins in inducing intestinal epithelial cell apoptosis and the attributed EGFR-STAT3 axis regulation.PLoS neglected tropical diseases · 2026Article
- STAT1-IFITM3 promotes autophagy in epithelial cells to controlLife science alliance · 2025Article
- Disruption of Epidermal Growth Factor Receptor Signaling in RPE Cells Increases Resistance to Ocular Toxoplasmosis.Investigative ophthalmology & visual science · 2025Article
- Inhibition of Src signaling induces autophagic killing of Toxoplasma gondii via PTEN-mediated deactivation of Akt.PLoS pathogens · 2025Article
- Potential role of host autophagy in Clonorchis sinensis infection.Parasitology research · 2024Article
- Crosstalk between integrin/FAK and Crk/Vps25 governs invasion of bovine mammary epithelial cells byiScience · 2023Article
- Article
- Overview of Apoptosis, Autophagy, and Inflammatory Processes inPathogens (Basel, Switzerland) · 2023Review
- Early immune and host cell responses toFrontiers in parasitology · 2023Article
- Autophagy in protists and their hosts: When, how and why?Autophagy reports · 2023Article
- Host cell proteins modulated upon Toxoplasma infection identified using proteomic approaches: a molecular rationale.Parasitology research · 2022Review
- B7-H4 reduction induced by Toxoplasma gondii infection results in dysfunction of decidual dendritic cells by regulating the JAK2/STAT3 pathway.Parasites & vectors · 2022Article
- Modulation of autophagy as a therapeutic strategy forFrontiers in cellular and infection microbiology · 2022Review
- Article
- Blood-brain barrier-restricted translocation ofeLife · 2021Article
- Lessons from Toxoplasma: Host responses that mediate parasite control and the microbial effectors that subvert them.The Journal of experimental medicine · 2021Review
- Infratentorial Stereotactic Biopsy of Brainstem and Cerebellar Lesions.Brain sciences · 2021Article
- Cryptosporidium parvum infection induces autophagy in intestinal epithelial cells.Cellular microbiology · 2021Article
- Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Targeting of Toxoplasma gondii by autophagy is an effective mechanism by which host cells kill the protozoan. Thus, the parasite must avoid autophagic targeting to survive. Here we show that the mammalian cytoplasmic molecule Focal Adhesion Kinase (FAK) becomes activated during invasion of host cells. Activated FAK appears to accompany the formation of the moving junction (as assessed by expression the parasite protein RON4). FAK activation was inhibited by approaches that impaired β1 and β3 integrin signaling. FAK caused activation of Src that in turn mediated Epidermal Growth Factor Receptor (EGFR) phosphorylation at the unique Y845 residue. Expression of Src-resistant Y845F EGFR mutant markedly inhibited ROP16-independent activation of STAT3 in host cells. Activation of FAK, Y845 EGFR or STAT3 prevented activation of PKR and eIF2α, key stimulators of autophagy. Genetic or pharmacologic inhibition of FAK, Src, EGFR phosphorylation at Y845, or STAT3 caused accumulation of the autophagy protein LC3 and LAMP-1 around the parasite and parasite killing dependent on autophagy proteins (ULK1 and Beclin 1) and lysosomal enzymes. Parasite killing was inhibited by expression of dominant negative PKR. Thus, T. gondii activates a FAK→Src→Y845-EGFR→STAT3 signaling axis within mammalian cells, thereby enabling the parasite to survive by avoiding autophagic targeting through a mechanism likely dependent on preventing activation of PKR and eIF2α.
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