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  The LMP1 promoter can be transactivated directly by NF-kappaB

Demetriades, C., & Mosialos, G. (2009). The LMP1 promoter can be transactivated directly by NF-kappaB. J Virol, 83(10), 5269-77. doi:10.1128/JVI.00097-09.

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Genre: Zeitschriftenartikel

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https://www.ncbi.nlm.nih.gov/pubmed/19279104 (beliebiger Volltext)
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 Urheber:
Demetriades, C.1, Autor           
Mosialos, G., Autor
Affiliations:
1Demetriades – Cell Growth Control in Health and Age-related Disease, Max Planck Research Groups, Max Planck Institute for Biology of Ageing, Max Planck Society, ou_3394001              

Inhalt

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Schlagwörter: Base Sequence Binding Sites Cell Line, Transformed Gene Expression Regulation, Viral Herpesvirus 4, Human/*genetics/metabolism Humans Molecular Sequence Data *Promoter Regions, Genetic Protein Binding Transcription Factor RelA/*metabolism *Transcriptional Activation Viral Matrix Proteins/*genetics
 Zusammenfassung: A bioinformatic analysis identified two putative NF-kappaB binding sites in the Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1) promoter. The ability of p65RelA to interact with the LMP1 promoter was shown by in vitro and in vivo assays. Using an EBV-transformed lymphoblastoid cell line as a reporter system for the activity of the +40/-328 LMP1 promoter region, the functional importance of NF-kappaB and other transcription factor binding sites was demonstrated. p65RelA could also induce LMP1 expression from the EBV genome in Daudi and P3HR1 Burkitt's lymphoma cell lines. Finally, it was shown that p65RelA could cooperate with EBNA2 or the aryl hydrocarbon receptor in the transactivation of the LMP1 promoter. Our study established the importance of NF-kappaB and several cis-acting elements in the regulation of the LMP1 promoter in a latency III environment and highlighted a complex interplay between NF-kappaB and other transcription factors in this process.

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 Datum: 2009-052009
 Publikationsstatus: Erschienen
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 Identifikatoren: Anderer: 19279104
DOI: 10.1128/JVI.00097-09
ISSN: 1098-5514 (Electronic)0022-538X (Linking)
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Titel: J Virol
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 83 (10) Artikelnummer: - Start- / Endseite: 5269 - 77 Identifikator: -