ArticleThe Journal of biological chemistry2011
The interferon-gamma-induced GTPase, mGBP-2, inhibits tumor necrosis factor alpha (TNF-alpha) induction of matrix metalloproteinase-9 (MMP-9) by inhibiting NF-kappaB and Rac protein.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 37 citations in OpenAlex.
- Molecular mechanisms and functions of guanylate-binding protein 2 in inflammation and cancer (Review).Oncology letters · 2025Review
- Guanylate binding proteins (GBPs) as novel therapeutic targets against single-stranded RNA viruses.Molecular biology reports · 2025Review
- From mechanisms to therapies: the multifaceted roles of guanylate-binding protein 2 in immunity, cancer, and beyond.Frontiers in immunology · 2025Review
- Selenium Mitigates Ammonia-Induced Neurotoxicity by Suppressing Apoptosis, Immune Imbalance, and Gut Microbiota-Driven Metabolic Disturbance in Fattening Pigs.Biological trace element research · 2023Article
- Article
- The Large GTPase, GBP-2, Regulates Rho Family GTPases to Inhibit Migration and Invadosome Formation in Breast Cancer Cells.Cancers · 2021Article
- Plasma GBP2 promoter methylation is associated with advanced stages in breast cancer.Genetics and molecular biology · 2020Article
- Review
- Guanylate-binding protein 2 regulates Drp1-mediated mitochondrial fission to suppress breast cancer cell invasion.Cell death & disease · 2017Article
- Up-regulation of GBP2 is Associated with Neuronal Apoptosis in Rat Brain Cortex Following Traumatic Brain Injury.Neurochemical research · 2017Article
- Matrix metalloproteinases in the brain and blood-brain barrier: Versatile breakers and makers.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2016Review
- Rho protein GTPases and their interactions with NFκB: crossroads of inflammation and matrix biology.Bioscience reports · 2014Review
- Identification of co-expressed gene signatures in mouse B1, marginal zone and B2 B-cell populations.Immunology · 2014Article
- Non-classical proIL-1beta activation during mammary gland infection is pathogen-dependent but caspase-1 independent.PloS one · 2014Article
- A yeast one-hybrid and microfluidics-based pipeline to map mammalian gene regulatory networks.Molecular systems biology · 2013Article
- miR-433 is aberrantly expressed in myeloproliferative neoplasms and suppresses hematopoietic cell growth and differentiation.Leukemia · 2013Article
- ADAM17 mediates MMP9 expression in lung epithelial cells.PloS one · 2013Article
- Taurine Reverses Atrial Structural Remodeling in Ach-CaclAdvances in experimental medicine and biologyArticle
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Matrix metalloproteinase-9 (MMP-9) is important in numerous normal and pathological processes, including the angiogenic switch during tumor development and tumor metastasis. Whereas TNF-α and other cytokines up-regulate MMP-9 expression, interferons (IFNs) inhibit MMP-9 expression. We found that IFN-γ treatment or forced expression of the IFN-induced GTPase, mGBP-2, inhibit TNF-α-induced MMP-9 expression in NIH 3T3 fibroblasts, by inhibiting MMP-9 transcription. The NF-κB transcription factor is required for full induction of MMP-9 by TNF-α. Both IFN-γ and mGBP-2 inhibit the transcription of a NF-κB-dependent reporter construct, suggesting that mGBP-2 inhibits MMP-9 induction via inhibition of NF-κB-mediated transcription. Interestingly, mGBP-2 does not inhibit TNF-α-induced degradation of IκBα or p65/RelA translocation into the nucleus. However, mGBP-2 inhibits p65 binding to a κB oligonucleotide probe in gel shift assays and to the MMP-9 promoter in chromatin immunoprecipitation assays. In addition, TNF-α activation of NF-κB in NIH 3T3 cells is dependent on Rac activation, as evidenced by the inhibition of TNF-α induction of NF-κB-mediated transcription by a dominant inhibitory form of Rac1. A role for Rac in the inhibitory action of mGBP-2 on NF-κB is further shown by the findings that mGBP-2 inhibits TNF-α activation of endogenous Rac and constitutively activate Rac can restore NF-κB transcription in the presence of mGBP-2. This is a novel mechanism by which IFNs can inhibit the cytokine induction of MMP-9 expression.
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Registered trials
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