ArticleProceedings of the National Academy of Sciences of the United States of America2013
Murine guanylate binding protein 2 (mGBP2) controls Toxoplasma gondii replication.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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Who cites it
126 citing papers in PubMed, 200 citations in OpenAlex.
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- Utilizing AI for the Identification and Validation of Novel Therapeutic Targets and Repurposed Drugs for Endometriosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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- From mechanisms to therapies: the multifaceted roles of guanylate-binding protein 2 in immunity, cancer, and beyond.Frontiers in immunology · 2025Review
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- Weighted gene co-expression network analysis identified GBP2 connected to PPARα activity and liver cancer.Scientific reports · 2024Article
- Mouse guanylate-binding proteins of the chromosome 3 cluster do not mediate antiviral activity in vitro or in mouse models of infection.Communications biology · 2024Article
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- Effective factors in the pathogenesis ofHeliyon · 2024Review
- IL-12 Mediates T-bet-Expressing Myeloid Cell-Dependent Host Resistance against Toxoplasma gondii.ImmunoHorizons · 2024Article
- iNOS is necessary for GBP-mediated T. gondii clearance in murine macrophages via vacuole nitration and intravacuolar network collapse.Nature communications · 2024Article
- Host E3 ubiquitin ligase ITCH mediatesmBio · 2024Article
- Deficiency in astrocyte CCL2 production reduces neuroimmune control of Toxoplasma gondii infection.PLoS pathogens · 2024Article
- IFNs in host defence and parasite immune evasion duringFrontiers in immunology · 2024Review
- Integrative modeling of guanylate binding protein dimers.Protein science : a publication of the Protein Society · 2023Article
66 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IFN-γ orchestrates the host response against intracellular pathogens. Members of the guanylate binding proteins (GBP) comprise the most abundant IFN-γ-induced transcriptional response. mGBPs are GTPases that are specifically up-regulated by IFN-γ, other proinflammatory cytokines, toll-like receptor agonists, as well as in response to Listeria monocytogenes and Toxoplasma gondii infection. mGBP2 localizes at the parasitophorous vacuole (PV) of T. gondii; however, the molecular function of mGBP2 and its domains in T. gondii infection is not known. Here, we show that mGBP2 is highly expressed in several cell types, including T and B cells after stimulation. We provide evidence that the C-terminal domain is sufficient and essential for recruitment to the T. gondii PV. Functionally, mGBP2 reduces T. gondii proliferation because mGBP2-deficient cells display defects in the replication control of T. gondii. Ultimately, mGBP2-deficient mice reveal a marked immune susceptibility to T. gondii. Taken together, mGBP2 is an essential immune effector molecule mediating antiparasitic resistance.
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