ArticleImmunology2011
Signal transducer and activator of transcription 1 negatively regulates constitutive gamma interferon-inducible lysosomal thiol reductase expression.
Article in Immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- TIGIT impairs NK cell antifibrotic activity through the IFNγ-IFI30 axis in schistosomiasis-induced liver fibrosis.Frontiers in immunology · 2026Article
- Interferon Gamma Inducible Protein 30: from biological functions to potential therapeutic target in cancers.Cellular oncology (Dordrecht, Netherlands) · 2024Review
- Post-Transcriptional Induction of the Antiviral Host Factor GILT/IFI30 by Interferon Gamma.International journal of molecular sciences · 2024Article
- Microglia express gamma-interferon-inducible lysosomal thiol reductase in the brains of Alzheimer's disease and Nasu-Hakola disease.Intractable & rare diseases research · 2018Article
- Regulation of ULK1 Expression and Autophagy by STAT1.The Journal of biological chemistry · 2017Article
- Diverse cellular and organismal functions of the lysosomal thiol reductase GILT.Molecular immunology · 2015Review
- Article
- Expanding roles for GILT in immunity.Current opinion in immunology · 2013Review
- Direct identification of an HPV-16 tumor antigen from cervical cancer biopsy specimens.Frontiers in immunology · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gamma interferon-inducible lysosomal thiol reductase (GILT) is an enzyme that catalyzes thiol bond reduction and plays an important role in the early steps of antigen processing. The key factor involved in the regulation of GILT expression upon cell stimulation with interferon-γ (IFN-γ) is signal transducer and activator of transcription 1 (STAT1). In this study, we examined the role of STAT1 in regulating the constitutive expression of GILT. We showed that STAT1 interacts with the GILT promoter, even in the absence of IFN-γ, and that STAT1 represses GILT expression. These results reveal an atypical negative regulatory role for STAT1 in the constitutive regulation of genes involved in antigen processing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.