ArticleMolecular and cellular biology2002
Repression by homeoprotein pitx1 of virus-induced interferon a promoters is mediated by physical interaction and trans repression of IRF3 and IRF7.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- MCRS1 sensitizes T cell-dependent immunotherapy by augmenting MHC-I expression in solid tumors.The Journal of experimental medicine · 2024Article
- Modulation of protease expression by the transcription factor Ptx1/PITX regulates protein quality control during aging.Cell reports · 2023Article
- PITX1 plays essential functions in cancer.Frontiers in oncology · 2023Review
- The transcription factor PITX1 drives astrocyte differentiation by regulating the SOX9 gene.The Journal of biological chemistry · 2020Article
- Hypersensitive IFN Responses in Lupus Keratinocytes Reveal Key Mechanistic Determinants in Cutaneous Lupus.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Article
- Pitx1 broadly associates with limb enhancers and is enriched on hindlimb cis-regulatory elements.Developmental biology · 2013Article
- The estrogen-regulated transcription factor PITX1 coordinates gene-specific regulation by estrogen receptor-alpha in breast cancer cells.Molecular endocrinology (Baltimore, Md.) · 2011Article
- Classical swine fever virus N(pro) limits type I interferon induction in plasmacytoid dendritic cells by interacting with interferon regulatory factor 7.Journal of virology · 2011Article
- MIP/Aquaporin 0 represents a direct transcriptional target of PITX3 in the developing lens.PloS one · 2011Article
- IRF-3 activation by Sendai virus infection is required for cellular apoptosis and avoidance of persistence.Journal of virology · 2008Article
- DUX4, a candidate gene of facioscapulohumeral muscular dystrophy, encodes a transcriptional activator of PITX1.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Cytokine regulation in SARS coronavirus infection compared to other respiratory virus infections.Journal of medical virology · 2006Article
- The POU transcription factor Oct-1 represses virus-induced interferon A gene expression.Molecular and cellular biology · 2005Article
- Group 13 HOX proteins interact with the MH2 domain of R-Smads and modulate Smad transcriptional activation functions independent of HOX DNA-binding capability.Nucleic acids research · 2005Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon A (IFN-A) genes are differentially expressed after virus induction. The differential expression of individual IFN-A genes is modulated by the specific transcription activators IFN regulatory factor 3 (IRF3) and IRF-7 and the homeoprotein transcription repressor Pitx1. We now show that repression by Pitx1 does not appear to be due to the recruitment of histone deacetylases. On the other hand, Pitx1 inhibits the IRF3 and IRF7 transcriptional activity of the IFN-A11 and IFN-A5 promoters and interacts physically with IRF3 and IRF7. Pitx1 trans-repression activity maps to specific C-terminal domains, and the Pitx1 homeodomain is involved in physical interaction with IRF3 or IRF7. IRF3 is able to bind to the antisilencer region of the IFN-A4 promoter, which overrides the repressive activity of Pitx1. These results indicate that interaction between the Pitx1 homeodomain and IRF3 or IRF7 and the ability of the Pitx1 C-terminal repressor domains to block IFN-A11 and IFN-A5 but not IFN-A4 promoter activities may contribute to our understanding of the complex differential transcriptional activation, repression, and antirepression of the IFN-A genes.
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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.