Cooperation of Stat2 and p300/CBP in signalling induced by interferon-α
Abstract
The transcription factor ISGF3 transduces interferon (IFN)-alpha signals and activates the transcription of cellular antiviral defence genes. Adenovirus E1A blocks the IFN-alpha response, allowing unhindered viral replication. ISGF3 consists of Stat1, Stat2 and p48. Here we show that p300 and/or CBP (CREB-binding protein), which are transcription adaptors targeted by E1A, interact specifically with Stat2. Binding occurs between the first cysteine-histidine-rich region of p300/CBP and the carboxy-terminal segment of Stat2, a domain essential for ISGF3 function. We find that this domain of Stat2 has transactivation potential, which correlates with its binding to p300/CBP. Moreover, E1A represses Stat2 transactivation and IFN-alpha-activated transcription by inhibiting p300/CBP function. This provides a new mechanism for inhibition of the IFN-alpha-activated antiviral response by E1A, and supports the view that E1A binding to p300/CBP has functional significance for adenovirus replication in its natural host.
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Although STATs bind a similar DNA binding site, they may interact with co-activators or co-repressors to regulate different sets of their own downstream targets.
“Although they bind to a similar DNA binding site, STATs may interact with co-activator or co-repressor to regulate different sets of their own downstream targets (5”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [44]
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- Authors
- Bhattacharya, S., Eckner, R., Grossman, S., Oldread, E., Arany, Z., D'Andrea, A., & Livingston, D. M.
- Affiliations
- Harvard University (US)
- Venue
- Nature
- Published
- 1996-09
- Volume
- 383
- Issue
- 6598
- Pages
- 344-347
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2013279950
- Cited by
- 493
- References
- 2
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 3 · 2023: 6 · 2022: 5 · 2021: 5 · 2020: 2 · 2019: 5 · 2018: 9 · 2017: 6 · 2016: 8 · 2015: 5 · 2014: 8 · 2013: 11 · 2012: 9
- FWCI
- 23.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- STAT2, P300, CREB-binding protein, ISGF3, STAT1, adenovirus E1A, transcriptional activation, protein-protein interaction, adenovirus replication
- MeSH terms
- Adenoviridae, Binding Sites, DNA-Binding Proteins, Gene Expression Regulation, HeLa Cells, Humans, Nuclear Proteins, Protein Binding, Transcription Factors, Tumor Cells, Cultured, Virus Replication, Signal Transduction, Trans-Activators, Interferon-alpha, Adenovirus E1A Proteins, STAT2 Transcription Factor, Interferon-Stimulated Gene Factor 3, Interferon-Stimulated Gene Factor 3, gamma Subunit, CREB-Binding Protein
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