Toxoplasma Gondii GRA35 Effector Mechanisms in Neuronal Apoptosis

A 2026 study by Jie Wang identifies the GRA35 protein as a key virulence factor driving neuronal apoptosis in Toxoplasmic encephalitis. The research compares wild-type ME49 T. gondii strains with GRA35 knockout variants, using GST-pull down, immunofluorescence, flow cytometry, and CCK8 assays. It demonstrates GRA35's dual role in triggering ER stress via the PERK pathway and promoting mitochondrial-associated apoptosis through interaction with RTN1-c.

Use Cases

• Compare neuronal apoptosis rates between wild-type ME49 and ME49Δgra35 strains using flow cytometry and CCK8 assay data.
• Analyze protein-protein interaction data from GST-pull down experiments to validate GRA35 binding with RTN1-c.
• Investigate the correlation between GRA35 expression and activation markers of the PERK signaling pathway from immunofluorescence data.
• Model the molecular cascade from ER stress to mitochondrial pathway-mediated apoptosis using the described experimental results.

Strengths

• Data is published under a permissive CC-BY-4.0 license.
• Study employs multiple experimental methods (GST-pull down, immunofluorescence, flow cytometry, CCK8) to validate findings.

Limitations

• Dataset is very small, consisting of 811.8 KB of DOC and PDF files containing research results, not raw data.
• No raw experimental data columns or sample data files are provided, limiting direct computational analysis.
• Findings are specific to the ME49 strain of Toxoplasma gondii and may not generalize to other strains.

Provenance

Source

Jie Wang via figshare.

Collection Method

Experimental biology comparing GRA35 gene knockout and wild-type T. gondii ME49 strains.

Time Range

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Freshness

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Geography

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