Transient expression of the beta interferon promoter in human cells.

Xanthoudakis, Steven; Alper, D; Hiscott, John

doi:10.1128/mcb.7.10.3830

Mol. Cell. Biol.

1987

DOI: 10.1128/mcb.7.10.3830

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Transient expression of the beta interferon promoter in human cells.

Steven Xanthoudakis¹,

D Alper²,

John Hiscott³

Abstract: 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; i… Show more

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Cited by 19 publications

(31 citation statements)

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“…NF-KB is a multisubunit transcription factor comprising p50, p65, and rel protooncogene products (7) that has been implicated in the regulation of the IFN-3 gene promoter by dsRNA (8)(9)(10). In many unstimulated cells, NF-KB is found localized to the cytoplasm as a latent heterodimeric complex bound to its subunit-specific inhibitor IKB (also called MAI)-3) (11).…”

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confidence: 99%

“…Human full-length PKR was expressed as a glutathione S-transferase (GST) fusion in the expression vector pGEX-2T and purified from bacteria by using glutathione-Sepharose chromatography (18). 1KB-a, p50, and p65 (10)(11)(12) were produced in a similarfashion except that the GST portion ofthese fusion proteins was cleaved with thrombin and removed by centrifugation (the molecular mass of the bacterially produced IKB-a protein was 37 kDa).…”

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Double-stranded RNA-dependent protein kinase activates transcription factor NF-kappa B by phosphorylating I kappa B.

Kumar

Haque

Lacoste

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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518

409

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The induction of interferon (IN) genes by viruses or double-stranded RNA (dsRNA) requires the assembly of a complex set of trnscription factors on responsive DNA elements of ION gene promoters. One of the factors necessary for regulating IFN-P gene transcription is nuclear factor NF-KB, the activation of which is triggered by dsRNA. It has previously been suggested that the dsRNA-activated p68 protein kinase (PKR) may act as an Inducer-receptor, transducing the signal from dsRNA to NF-ucB through phosphorylation of the inhibitor IKB. We present direct evidence that PKR can phosphorylate IKB-a (MAD-3) and activate NF-KB DNA binding activity in vitro. We further show that dsRNA induces an unusual phosphorylated form of IKB-a. The expression of a transdominant mutant PKR is able to perturb the dsRNAmediated signaling pathway in vivo, suggesting a role for this kinase in IFN-P gene induction.

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mentioning

confidence: 99%

mentioning

confidence: 99%

Double-stranded RNA-dependent protein kinase activates transcription factor NF-kappa B by phosphorylating I kappa B.

Kumar

Haque

Lacoste

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

518

409

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show abstract

“…We previously described a human transient expression system that accurately reflected the virus-induced activation of the IFN-P promoter (49). Expression of IFN-,-Bchloramphenicol acetyltransferase (CAT) hybrid genes was dependent on induction by virus; however, no expression from the IFN-a-CAT hybrid gene was detectable, indicating that human epithelioid cells lack a factor required for the expression of the IFN-a promoter.…”

mentioning

confidence: 99%

“…TAg also increases production of mRNA from other viral and cellular promoters (1,6,40). We asked whether TAg could likewise trans activate by similar indirect mechanisms the IFN promoter, given that IFN regulation is tightly controlled by positive and negative regulatory interactions (9,13,27,49,51). The activities of the IFN-a1 and IFN-, promoters were first compared in the presence and absence of viral TAg (Fig.…”

mentioning

confidence: 99%

trans activation of type 1 interferon promoters by simian virus 40 T antigen.

Hiscott¹,

Wong²,

Alper³

et al. 1988

Mol. Cell. Biol.

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A human transient expression system was used to measure the influence of simian virus 40 T antigen and adenovirus Ela proteins on the activation of alpha interferon subtype 1 (IFN-a,) and IFN-1 promoters linked to the reporter chloramphenicol acetyltransferase gene. Large T-antigen production, amplified by expression plasmid replication in transfected 293 cells, was able to trans activate the IFN-, promoter 5-to 10-fold, increasing both the constitutive and Sendai virus-induced levels of expression. Surprisingly, the previously quiescent transfected IFN-ae promoter in T-antigen-expressing cells displayed a level of inducibility similar to (8,15,20,33,37). The IFN-P regulatory sequences between positions -77 and -37 relative to the mRNA CAP site comprise an inducible enhancer element, with overlapping positive and negative regulatory domains (13-15); the 5' boundary of sequences required for induction may however vary depending on the cell type (8,15). A hexanucleotide repeat (consensus AAGTGA), permutations of which are present throughout the -65 to -109 region of the IFN-P promoter, has been shown to confer virus-induced transcriptional activation to homologous or heterologous promoters (9). Similarly, an IFN-a1 promoter fragment from positions -109 to -64 conferred virus inducibility to a rabbit P-globin promoter segment (39); in addition, a GAAAGPy hexameric repeat possessed the ability to suppress the activity of constitutive enhancer elements (27). tions -68 and -38 and positions -167 to -94. After virus induction, the interferon-regulatory element-binding proteins were at least partially dissociated and replaced by a factor binding to sequences located between positions -77 and -64 (51). Similarly, a gel electrophoresis DNA-binding assay identified an IFN-specific protein in uninduced myeloid KG-1 cells interacting with the upstream region of the IFN-,B promoter (50).We previously described a human transient expression system that accurately reflected the virus-induced activation of the IFN-P promoter (49). Expression of IFN-,-Bchloramphenicol acetyltransferase (CAT) hybrid genes was dependent on induction by virus; however, no expression from the IFN-a-CAT hybrid gene was detectable, indicating that human epithelioid cells lack a factor required for the expression of the IFN-a promoter. In the present study, we demonstrate that both the IFN-P and the previously silent

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“…The positive regulatory domain I (PRDI) is located between nucleotides -77 and -64 from the start site of transcription, while another element (PRDII) is located between -66 and -55 (7)(8)(9)(10). A third element (PRDIII) is located between -90 and -78 (11)(12)(13)(14)(15).…”

mentioning

confidence: 99%

An ATF/CREB binding site is required for virus induction of the human interferon beta gene [corrected]

Maniatis

1992

Proc. Natl. Acad. Sci. U.S.A.

105

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We report the characterization of a distinct regulatory element of the human interferon (3 (HuIFN-(3) gene promoter, which we designate PRDIV (positive regulatory domain IV). In previous studies, sequences between -104 and -91 base pairs upstream from the start site of transcription were shown to be required for maximal levels of virus induction in mouse L929 cells. We have localized the essential sequence in this region extending from -99 to at least -91, and we show that this sequence is a binding site for a protein of the activating transcription factor/cAMP response element binding protein (ATF/CREB) family of transcription factors. Mutations in PRDIV that decrease the affinity of one member of this family (ATF-2/CRE-BP1) decrease the level of virus induction in vivo.

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Transient expression of the beta interferon promoter in human cells.

Cited by 19 publications

References 7 publications

Double-stranded RNA-dependent protein kinase activates transcription factor NF-kappa B by phosphorylating I kappa B.

Double-stranded RNA-dependent protein kinase activates transcription factor NF-kappa B by phosphorylating I kappa B.

trans activation of type 1 interferon promoters by simian virus 40 T antigen.

An ATF/CREB binding site is required for virus induction of the human interferon beta gene [corrected]

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