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<i>Toxoplasma gondii</i> effector GRA35 mediates neuronal damage <i>via</i> ER stress and mitochondria-associated apoptosis.

Overview

Authors: Jie Wang1,2, Ying Chen2,3, Nan Zhou1,2, Fangmin Li1,2, Niuniu Dai1,2, Zhiang Chen1,2, Shutong Liu1, Ran An1,2, Lijian Chen4, Jian Du1,2,4
ORCID iDs: Jian Du
  1. Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China
  2. The Provincial Key Laboratory of Zoonoses of High Institutions in Anhui, Anhui Medical University, Hefei, China
  3. School of Nursing, Anhui Medical University, Hefei, China
  4. Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, China
Institutions: Anhui Medical University (China); First Affiliated Hospital of Anhui Medical University (China)
Journal: Virulence, volume 17, issue 1, article 2654261
Dates: published online 6 April 2026; in print December 2026
Type: Research article · Language: English
License: CC BY
Identifiers: DOI 10.1080/21505594.2026.2654261 · PMID 41940502 · PMCID PMC13078242 · OpenAlex W7151042733
Open access: gold, a free copy (OpenAlex)
Status: data only
Categories: human (organism), mouse (organism), other condition (population), cellular / molecular (subfield)
Methods: Statistics
Keywords: Toxoplasma gondii, GRA35, RTN1-c, encephalitis, apoptosis
MeSH: Apoptosis*, Endoplasmic Reticulum Stress*, Mitochondria*, Neurons*, Protozoan Proteins*, Toxoplasma*, Animals, Brain, Gene Knockout Techniques, Humans, Mice, Signal Transduction, Virulence Factors (* major topic)
Journal subjects: Host Response
Topic: Toxoplasma gondii Research Studies (Parasitology, Immunology and Microbiology), according to OpenAlex
Funding: National Natural Science Foundation of China (82472313)
Citations: cited by 2 papers (Europe PMC); 42 references in the paper

Abstract

Encephalitis resulting from acute reactivation of chronic Toxoplasma gondii infection in the central nervous system poses a significant mortality risk in immunodeficient individuals. However, the specific molecular mechanisms underlying this process remain elusive. We constructed the GRA35 gene knockout ME49 strain and compared the differences with wild type ME49 strain. We used the GST-pull down experiment to explore the mechanism of GRA35 promoting neuronal cell apoptosis. We used immunofluorescence, flow cytometry and CCK8 experiments to verify the pathway of GRA35 promoting neuronal cell apoptosis. Our study reveals that wild type ME49 strain promotes neuronal apoptosis in brain following chronic infection activation. Conversely, infection with the ME49Δgra35 strain leads to a reduced apoptotic response in brain neurons. Furthermore, we demonstrate that GRA35 interacts with RTN1-c, thereby promoting mitochondrial pathway-mediated apoptosis in neurons. Additionally, GRA35 can trigger host cell ER stress-associated apoptosis through the PERK signaling pathway. GRA35 serves as a crucial virulence factor in the pathogenesis of Toxoplasmic encephalitis (TE), which offers potential new therapeutic target and theoretical insights for TE.

Reproduced under the paper's license (CC BY), from the paper cited above.

Code

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Data

Datasets cited

Data availability statement

The mass spectrometry raw data of Figure 5 are openly available in the ScienceDB (https://doi.org/10.57760/sciencedb.29128 [41]) and in the ProteomeXchange database at https://www.ebi.ac.uk/pride/archive/projects/PXD067653, accession number PXD067653. The data that support the findings of this study are openly available in figshare at (http://doi.org/10.6084/m9.figshare.29329469 [42]).

Reproduced under the paper's license (CC BY), from the paper cited above.

Versions

The history of this record: each version stored by the harvester or made by a correction of its authors or of the maintainers of its code, and what changed in its facts. The texts of the paper (its abstract, its availability statements) are not part of it; versions that changed only those are not listed.

Version 1, 29 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 10 authors, 5 keywords, 13 MeSH terms, 1 funder, 42 references.

Cite

This paper

Wang, J., Chen, Y., Zhou, N., Li, F., Dai, N., Chen, Z., Liu, S., An, R., Chen, L., & Du, J. (2026). <i>Toxoplasma gondii</i> effector GRA35 mediates neuronal damage <i>via</i> ER stress and mitochondria-associated apoptosis. Virulence, 17(1), 2654261. https://doi.org/10.1080/21505594.2026.2654261

BibTeX

@article{wang2026lt,
author = {Wang, Jie and Chen, Ying and Zhou, Nan and Li, Fangmin and Dai, Niuniu and Chen, Zhiang and Liu, Shutong and An, Ran and Chen, Lijian and Du, Jian},
title = {{\<i\>Toxoplasma gondii\</i\> effector GRA35 mediates neuronal damage \<i\>via\</i\> ER stress and mitochondria-associated apoptosis}},
journal = {Virulence},
year = {2026},
month = apr,
volume = {17},
number = {1},
pages = {2654261},
publisher = {Taylor \& Francis},
issn = {2150-5594},
doi = {10.1080/21505594.2026.2654261},
url = {https://doi.org/10.1080/21505594.2026.2654261},
pmid = {41940502},
pmcid = {PMC13078242}
}

RIS

TY - JOUR
AU - Wang, Jie
AU - Chen, Ying
AU - Zhou, Nan
AU - Li, Fangmin
AU - Dai, Niuniu
AU - Chen, Zhiang
AU - Liu, Shutong
AU - An, Ran
AU - Chen, Lijian
AU - Du, Jian
TI - <i>Toxoplasma gondii</i> effector GRA35 mediates neuronal damage <i>via</i> ER stress and mitochondria-associated apoptosis
T2 - Virulence
J2 - Virulence
PY - 2026
DA - 2026/04/10
VL - 17
IS - 1
SP - 2654261
SN - 2150-5594
PB - Taylor & Francis
DO - 10.1080/21505594.2026.2654261
UR - https://doi.org/10.1080/21505594.2026.2654261
LA - en
ER -

CSL-JSON

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