Cloning and partial characterization of the promoter for the human p55 tumor necrosis factor (TNF) receptor

Kemper, Oliver; Wallach, David

doi:10.1016/0378-1119(93)90095-k

Cited by 44 publications

(35 citation statements)

References 48 publications

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“…A great deal of research has focused on posttranscriptional and posttranslational regulation of TNF-R1; in contrast, very little is known about the regulation of the TNF-R1 promoter. A 5Ј region upstream of the TNF-R1 start codon has been shown to encode promoter activity, and the transcriptional start sites have been determined (18). In order to investigate the effect of BZLF1 on TNF-R1 promoter activity, a TNF-R1-CAT reporter plasmid was constructed by PCR cloning of a 654-bp region from the human genome corresponding to the Ϫ619/ ϩ35 region of the TNF-R1 promoter (relative to the major transcriptional start site), as previously defined (18).…”

Section: Epstein-barr Virus (Ebv) Is a Ubiquitous Human ␥-Herpes-mentioning

confidence: 99%

“…A 5Ј region upstream of the TNF-R1 start codon has been shown to encode promoter activity, and the transcriptional start sites have been determined (18). In order to investigate the effect of BZLF1 on TNF-R1 promoter activity, a TNF-R1-CAT reporter plasmid was constructed by PCR cloning of a 654-bp region from the human genome corresponding to the Ϫ619/ ϩ35 region of the TNF-R1 promoter (relative to the major transcriptional start site), as previously defined (18). These sequences were inserted upstream of the chloramphenicol acetyltransferase (CAT) reporter gene, and the resulting plasmid was used in cotransfection assays.…”

Section: Epstein-barr Virus (Ebv) Is a Ubiquitous Human ␥-Herpes-mentioning

confidence: 99%

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Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

Morrison

Mauser

Klingelhutz

et al. 2004

J Virol

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Tumor necrosis factor alpha (TNF-␣) is a key mediator of host immune and inflammatory responses and inhibits herpesvirus replication by cytolytic and noncytolytic mechanisms. TNF-␣ effects are primarily mediated through the major TNF-␣ receptor, TNF-R1, which is constitutively expressed in most cell types. Here we show that the Epstein-Barr virus (EBV) immediate-early protein BZLF1 prevents TNF-␣ activation of target genes and TNF-␣-induced cell death. These effects are mediated by down-regulation of the promoter for TNF-R1. Additionally, we demonstrate that expression of TNF-R1 is downregulated during the EBV lytic replication cycle. Thus, EBV has developed a novel mechanism for evading TNF-␣ antiviral effects during lytic reactivation or primary infection.

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Section: Epstein-barr Virus (Ebv) Is a Ubiquitous Human ␥-Herpes-mentioning

confidence: 99%

Section: Epstein-barr Virus (Ebv) Is a Ubiquitous Human ␥-Herpes-mentioning

confidence: 99%

Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

Morrison

Mauser

Klingelhutz

et al. 2004

J Virol

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show abstract

“…From the published sequences 14,15 (GENBANK NID: 339746 and 288493), 16 PCR fragments were generated. In all, 596 bp were screened in the 5 0 region, 211 bp in the 5 0 UTR region, 1368 bp in the coding sequence, 1056 bp in the intronic regions flanking exons and 541 bp in the 3 0 UTR region.…”

Section: Identification Of Polymorphismsmentioning

confidence: 99%

Polymorphism R92Q of the tumour necrosis factor receptor 1 gene is associated with myocardial infarction and carotid intima-media thickness – The ECTIM, AXA, EVA and GENIC Studies

et al. 2003

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The TNFRSF1A gene was screened for polymorphisms in 95 subjects with premature myocardial infarction (MI), who also had one parent who had an MI. A total of 10 polymorphisms were found: three in the promoter region, two in exons and five in introns. All polymorphisms were genotyped in ECTIM, a case-control study of MI (1815 subjects). The nonsynonymous 92Q allele was found in 1.8, 1.0 and 1.7% of controls from Strasbourg, Belfast and Glasgow -respectively; in cases: 4.2, 2.2 and 3.2%. The populationadjusted odds ratio (OR) for MI associated with allele Q carrying was 2.15 (95% CI: 1.09 -4.23). To check its possible implication in atherosclerosis, this polymorphism was then genotyped in the AXA Study (ultrasound examinations of carotid and femoral arteries in the context of an employment medical examination, 733 subjects), the EVA Study (ultrasound examinations of carotid arteries in a study of cognitive and vascular ageing, 1092 subjects) and the GENIC Study (on brain infarction (BI), 912 subjects). In the AXA Study, among smokers, carrying the 92Q allele was positively associated with the presence of a carotid plaque (OR 5.07; 95% CI: 1.64 -15.63) and with a thickening of the carotid intima-media thickness (IMT) (0.59 (0.11) vs 0.54 (0.11), P ¼ 0.045). In the EVA Study, carriers of allele 92Q had an increased mean carotid IMT (0.70 (0.09) vs 0.67 (0.13), P ¼ 0.02). No significant association of the 92Q allele was found with BI in the GENIC Study. Overall, these results may suggest that carriers of the 92Q allele may be at increased risk of atherosclerosis.

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“…However, the mechanism for this effect has not been defined. To date, relatively little is known about how the TNFR1 promoter is normally regulated (35,67,72). However, our laboratory recently demonstrated that the promoter contains a C/EBP binding site and showed that both C/EBP␣ and C/EBP␤ bind to and activate the TNFR1 promoter (7).…”

mentioning

confidence: 99%

The Epstein-Barr Virus BZLF1 Protein Inhibits Tumor Necrosis Factor Receptor 1 Expression through Effects on Cellular C/EBP Proteins

Bristol

Robinson²,

Barlow³

et al. 2010

J Virol

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The Epstein-Barr virus immediate-early protein, BZLF1 (Z), initiates the switch between latent and lytic infection and plays an essential role in mediating viral replication. Z also inhibits expression of the major receptor for tumor necrosis factor (TNF), TNFR1, thus repressing TNF cytokine signaling, but the mechanism for this effect is unknown. Here, we demonstrate that Z prevents both C/EBP␣-and C/EBP␤-mediated activation of the TNFR1 promoter (TNFR1p) by interacting directly with both C/EBP family members. We show that Z interacts directly with C/EBP␣ and C/EBP␤ in vivo and that a Z mutant altered at alanine residue 204 in the bZIP domain is impaired for the ability to interact with both C/EBP proteins. Furthermore, we find that the Z(A204D) mutant is attenuated in the ability to inhibit the TNFR1p but mediates lytic viral reactivation and replication in vitro in 293 cells as well as wild-type Z. Although Z does not bind directly to the TNFR1p in EMSA studies, chromatin immunoprecipitation studies indicate that Z is complexed with this promoter in vivo. The Z(A204D) mutant has reduced interaction with the TNFR1p in vivo but is similar to wild-type Z in its ability to complex with the IL-8 promoter. Finally, we show that the effect of Z on C/EBP␣-and C/EBP␤-mediated activation is promoter dependent. These results indicate that Z modulates the effects of C/EBP␣ and C/EBP␤ in a promoter-specific manner and that in some cases (including that of the TNFR1p), Z inhibits C/EBP␣-and C/EBP␤-mediated activation.

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Cloning and partial characterization of the promoter for the human p55 tumor necrosis factor (TNF) receptor

Cited by 44 publications

References 48 publications

Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

Epstein-Barr Virus Immediate-Early Protein BZLF1 Inhibits Tumor Necrosis Factor Alpha-Induced Signaling and Apoptosis by Downregulating Tumor Necrosis Factor Receptor 1

Polymorphism R92Q of the tumour necrosis factor receptor 1 gene is associated with myocardial infarction and carotid intima-media thickness – The ECTIM, AXA, EVA and GENIC Studies

The Epstein-Barr Virus BZLF1 Protein Inhibits Tumor Necrosis Factor Receptor 1 Expression through Effects on Cellular C/EBP Proteins

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