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Synergism between multiple virus-induced factor-binding elements involved in the differential expression of interferon A genes.

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TLDR
It is shown that the low levels of IFN-A11 gene expression are caused essentially by the lack of two inducible enhancer domains disrupted by the A−78 → G and the G−57 → C substitutions, and suggested that virus-induced factor may correspond to the primary transcription factor directly activated by virus that is involved in the initiation of IFn-A gene transcription.
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This article is published in Journal of Biological Chemistry.The article was published on 1997-08-29 and is currently open access. It has received 39 citations till now. The article focuses on the topics: Enhancer & Promoter.

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Differential viral induction of distinct interferon-α genes by positive feedback through interferon regulatory factor-7

TL;DR: It is reported that the large family of IFNα genes can be divided into two groups: an immediate‐early response gene (IFNα4) which is induced rapidly and without the need for ongoing protein synthesis; and a set of genes that display delayed induction, which are induced more slowly and require cellular protein synthesis.
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Virus-Dependent Phosphorylation of the IRF-3 Transcription Factor Regulates Nuclear Translocation, Transactivation Potential, and Proteasome-Mediated Degradation

TL;DR: Interestingly, virus infection resulted in the association of IRF-3 with the CREB binding protein (CBP) coactivator, as detected by coimmunoprecipitation with anti-CBP antibody, an interaction mediated by the C-terminal domains of both proteins.
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Interferon regulatory factors: the next generation.

TL;DR: The aim of this review is to provide an update on the novel discoveries in the area of IRF transcription factors and the important roles of the new generation of IRFs--particularly IRF-3, IRf-4 andIRF-7.
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The growing family of interferon regulatory factors

TL;DR: Understanding the molecular mechanisms by which the IRFs affect these important cellular events and IFN expression will contribute to a greater understanding of events leading to various viral, immune and malignant disease states and will suggest novel strategies for antiviral and immune modulatory therapy.
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Regulation of the type I IFN induction: a current view

TL;DR: The type I IFN-alpha/beta gene family was identified about a quarter of a century ago as a prototype of many cytokine gene families, which led to the subsequent burst of studies on molecular mechanisms underlying cytokin gene expression and signaling.
References
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Journal ArticleDOI

Accurate transcription initiation by RNA polymerase II in a soluble extract from isolated mammalian nuclei

TL;DR: A procedure for preparing extracts from nuclei of human tissue culture cells that directs accurate transcription initiation in vitro from class II promoters, including tRNA and Ad 2 VA, is developed.
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Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins

TL;DR: A previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that phosphorylate substrate proteins called STATs (signal transducers and activators of transcription).
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CAT constructions with multiple unique restriction sites for the functional analysis of eukaryotic promoters and regulatory elements

TL;DR: In the promoterless construction pBLCAT3 eight unique restriction sites are suitable for insertion of different eukaryotic promoters at the 5' end of the CAT gene, enabling the excision of the intact fusion gene from the prokaryotic vector.
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A nuclear factor for IL-6 expression (NF-IL6) is a member of a C/EBP family.

TL;DR: Interestingly, NF‐IL6 was shown to bind to the regulatory regions for various acute‐phase protein genes and several other cytokine genes such as TNF, IL‐8 and G‐CSF, implying that NF‐ IL6 has a role in regulation not only for the IL‐6 gene but also for several other genes involved in acute‐ phase reaction, inflammation and hemopoiesis.
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Virus induction of human IFNβ gene expression requires the assembly of an enhanceosome

TL;DR: Evidence that transcriptional activation of the human interferon-beta (IFN beta) gene requires the assembly of a higher order transcription enhancer complex (enhanceosome) is presented and HMG I(Y) plays an essential role in the assembly and function of the IFN beta gene enhanceosome.
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