A human IFN-<i>β</i><sub>1</sub>, gene deleted of promoter sequences upstream from the TATA box is controlled post-transcriptionally by dsRNA

Nir, Uri; Cohen, Batya; Chen, Louisa; Revel, Michel

doi:10.1093/nar/12.18.6979

Cited by 35 publications

(17 citation statements)

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“…However, the mechanism for IFN priming is not yet well understood. The stimulation of IFN production observed upon priming is known from an increase in the rate of IFN gene transcription and requires an IFN-inducible factor(s) (17,18). It seems likely that IRF-7 is an important factor in priming action of IFN because IRF-7 is inducible by IFN and IRF-7 is responsible for the robust and wide variety of type I IFN production (23,55).…”

Section: Discussionmentioning

confidence: 99%

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The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Brumm

Zhang

2006

Journal of Biological Chemistry

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Epstein-Barr virus (EBV)3 is a human ␥ herpesvirus and is an important cause of lymphomas in patients with advanced human immunodeficiency virus infection or AIDS and in severely immunocompromised people, especially organ transplant recipients. Also, EBV infection is associated with the development of nasopharyngeal carcinoma and Burkitt's lymphoma (BL) (1, 2).The biologic hallmark of EBV-cell interaction is latency. Three types of latency have been described, each having its own distinct pattern of gene expression. Type I latency is exemplified by BL tumors in vivo. EBV nuclear antigen 1 (EBNA-1) protein is expressed in this form of latency. Type II latency is exemplified by nasopharyngeal carcinoma and Hodgkin disease. EBNA-1, latent membrane protein 1 (LMP-1), and LMP2A and LMP2B proteins are expressed in type II latency. Type III latency is represented by lymphoblastoid cell lines. Nine viral proteins are expressed, including six nuclear proteins (EBNA-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, and EBNA-LP) and three integral membrane proteins (LMP-1, LMP-2A, and LMP-2B) (reviewed in Refs. 1 and 2).EBV LMP-1 is the principal oncoprotein required for EBV transformation of human B cells and establishment of latency in vitro. LMP-1 is an integral membrane protein with six transmembrane-spanning domains with a long C-terminal domain, which is located in the cytoplasm (2, 3). Two C-terminal activator regions (CTARs) have been identified to initiate signal transduction. LMP-1 acts as a constitutively active receptor-like molecule that does not need the binding of a ligand (4). LMP-1 appears to be a central effector of altered cell growth, survival, adhesive, invasive, and antiviral potential (5-9).Type I interferons (IFNs) are cytokines with many functions including antiviral and anti-proliferation (10, 11). IFNs are produced upon the infection of cells by viruses. There are a large number of type I IFN genes in the human: 13 IFN-␣ genes, 1 IFN-␤ gene, and 1 IFN-gene (12). It is not known now why there are so many type I IFN genes. However, a unique role for IFN-␤ for a fully effective antiviral response, which cannot be compensated by IFN-␣, has been documented (13).The amount of IFNs produced by viruses or double-stranded RNA can be increased robustly by treating cells with IFN before infection, a phenomenon known as IFN priming (14 -16). The stimulation of IFN production observed upon priming results from an increase in the rate of IFN gene transcription and requires an IFN-inducible factor(s) (17,18).The mechanism of the transcriptional activation of IFNs has been under intensive investigation. One of the major players in the IFN production is IFN regulatory factor 7 (IRF-7). IRF-7 was cloned in the context of EBV latency and has an intimate relation with EBV (19 -25). IRF-7 is inducible by type I IFNs and can be further activated by phosphorylation and nuclear translocation upon viral infection, and activated IRF-7 is partially responsible for the robust transcriptional activation of IFNs (23,[26][27][28][29].Prev...

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Section: Discussionmentioning

confidence: 99%

“…The stimulation of IFN production observed upon priming results from an increase in the rate of IFN gene transcription and requires an IFN-inducible factor(s) (17,18).…”

Section: Epstein-barr Virus (Ebv)mentioning

confidence: 99%

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Brumm

Zhang

2006

Journal of Biological Chemistry

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“…In the absence of induction, P-IFN mRNA is usually undetectable; however, upon induction as many as 5,000 ,B-IFN mRNA transcripts can accumulate per cell. The induction is due at least in part to an increase in the rate of transcription of the p-IFN gene (35,37; K. Zinn, Ph.D. thesis, Harvard University, Cambridge, Mass. 1983).…”

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confidence: 99%

“…Priming can increase IFN production by up to 20-fold in cell lines in which it is observed (19,25,43,44), and in some cases it can also accelerate the kinetics of IFN induction (1,15,18). The stimulation of IFN production observed upon priming results from an increase in the rate of P-IFN gene transcription (35).…”

mentioning

confidence: 99%

Activation of the human beta-interferon gene requires an interferon-inducible factor.

Enoch¹,

Zinn²,

Maniatis³

1986

Mol. Cell. Biol.

233

133

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beta-Interferon (beta-IFN) gene expression can be induced by poly(I)-poly(C) or virus, but there is considerable variation in the extent of induction between different cell lines. We characterized two poorly inducible human cell lines, HeLa and 143 thymidine kinase negative (143 tk-), to define cellular factors involved in the activation of the beta-IFN gene. We show that the deficiency in beta-IFN induction in these cells can be complemented by fusion to highly inducible mouse cells. We conclude that the human cells are deficient in a trans-acting factor required for B-IFN gene activation. The level of induction of the beta-IFN gene in HeLa and 143 tk- cells can also be increased by priming with IFN before induction. If IFN priming is carried out in the presence of cycloheximide, a approximately 200-fold increase in induction is observed. We conclude that activation of the beta-IFN gene requires an IFN-inducible factor that is only expressed at low levels in unprimed HeLa and 143 tk- cells.

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“…Recently, an elegant study has demonstrated that the IFN-,B enhancer element is negatively regulated and has identified regions of the IFN-13 promoter to which putative regulatory factors bind (7,34). In addition to sequences required for transcriptional activation at the 5' flanking end of the gene, sequences at the 3' untranslated end of the gene and mRNA are involved in RNA stability and turnover (23,24,27 (Fig. 3).…”

mentioning

confidence: 99%

Transient expression of the beta interferon promoter in human cells.

Xanthoudakis¹,

Alper²,

Hiscott³

1987

Mol. Cell. Biol.

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A human transient expression assay was used to examine the inducible transcriptional activation of beta interferon (IFN-beta) and IFN-alpha 1 promoters in a homologous cellular environment. Use of 293 cells, an adenovirus DNA-transformed human embryonic kidney cell line, permitted Sendai virus-inducible expression of IFN-beta-CAT hybrid gene. Introduction of the simian virus 40 (SV40) enhancer 5' or 3' to the IFN-CAT gene increased basal (uninduced) levels of chloramphenicol acetyltransferase (CAT) activity; in one construct the SV40 enhancer--IFN-beta regulatory region combination increased the induced CAT activity 50- to 100-fold, suggesting that this may be a generally useful inducible enhancer-promoter combination. No expression from the IFN-alpha-CAT hybrid gene was detected in 293 cells, indicating that human epithelioid cells lack a factor required for expression of the IFN-alpha promoter. However, when the IFN-alpha regulatory region was combined with the SV40 enhancer, a low level of inducible CAT activity was detected in the human transient system.

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A human IFN-β₁, gene deleted of promoter sequences upstream from the TATA box is controlled post-transcriptionally by dsRNA

Cited by 35 publications

References 35 publications

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Activation of the human beta-interferon gene requires an interferon-inducible factor.

Transient expression of the beta interferon promoter in human cells.

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A human IFN-β1, gene deleted of promoter sequences upstream from the TATA box is controlled post-transcriptionally by dsRNA

Cited by 35 publications

References 35 publications

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

The Latent Membrane Protein 1 of Epstein-Barr Virus (EBV) Primes EBV Latency Cells for Type I Interferon Production

Activation of the human beta-interferon gene requires an interferon-inducible factor.

Transient expression of the beta interferon promoter in human cells.

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Product

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About

A human IFN-β₁, gene deleted of promoter sequences upstream from the TATA box is controlled post-transcriptionally by dsRNA