The High Mobility Group protein HMG I(Y) is required for NF-κB-dependent virus induction of the human IFN-β gene
Abstract
In this paper, we show that both NF-kappa B and the high mobility group protein I(Y) (HMG I(Y)) are required for virus induction of the human interferon-beta (IFN-beta) gene. NF-kappa B binds to the terminal regions of a 10 bp regulatory sequence through contacts in the major groove. while HMG I(Y) recognizes the central region of the same sequence through contacts in the minor groove. Mutations that interfere with binding of either protein decrease the level of virus induction, and activation of the gene can be blocked by either NF-kappa B or HMG I(Y) antisense RNA. HMG I(Y) stimulates the binding of NF-kappa B to the IFN-beta promoter, and it may also function as a promoter-specific accessory factor for NF-kappa B transcriptional activity.
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HMGA1 enhances NF-κB binding, as in the case of the IFN1-γ promoter.
“HMGA1 has been observed to enhance NF-κB binding, as in the case of the IFN1-γ promoter (Thanos et al., 1992).”
From Evidence for miR‐181 involvement in neuroinflammatory responses of astrocytes (2013) · cites this paper as Thanos et al., 1992
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- Authors
- Thanos, D., & Maniatis, T.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1992-11
- Volume
- 71
- Issue
- 5
- Pages
- 777-789
- ISSN
- 0092-8674
- Cited by
- 475
- References
- 0
- Language
- en
- Funders
- National Institutes of Health (Al20642)
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