دورية أكاديمية
The varicella-zoster virus immediate-early 63 protein affects chromatin-controlled gene transcription in a cell-type dependent manner.
العنوان: | The varicella-zoster virus immediate-early 63 protein affects chromatin-controlled gene transcription in a cell-type dependent manner. |
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المؤلفون: | Habran, Lionel, El Mjiyad, Nadia, Di Valentin, Emmanuel, Sadzot-Delvaux, Catherine, Bontems, Sébastien, Piette, Jacques |
المساهمون: | GIGA-I3 - Giga-Infection, Immunity and Inflammation - ULiège |
المصدر: | BMC Molecular Biology, 8, 99 (2007-10) |
بيانات النشر: | BioMed Central |
سنة النشر: | 2007 |
المجموعة: | University of Liège: ORBi (Open Repository and Bibliography) |
مصطلحات موضوعية: | Varicella zoster virus, NF-KB, Life sciences, Biochemistry, biophysics & molecular biology, Sciences du vivant, Biochimie, biophysique & biologie moléculaire |
الوصف: | peer reviewed ; Varicella Zoster Virus Immediate Early 63 protein (IE63) has been shown to be essential for VZV replication, and critical for latency establishment. The activity of the protein as a transcriptional regulator is not fully clear yet. Using transient transfection assays, IE63 has been shown to repress viral and cellular promoters containing typical TATA boxes by interacting with general transcription factors. In this paper, IE63 regulation properties on endogenous gene expression were evaluated using an oligonucleotide-based micro-array approach. We found that IE63 modulates the transcription of only a few genes in HeLa cells including genes implicated in transcription or immunity. Furthermore, we showed that this effect is mediated by a modification of RNA POL II binding on the promoters tested and that IE63 phosphorylation was essential for these effects. In MeWo cells, the number of genes whose transcription was modified by IE63 was somewhat higher, including genes implicated in signal transduction, transcription, immunity, and heat-shock signalling. While IE63 did not modify the basal expression of several NF-κB dependent genes such as IL-8, ICAM-1, and IκBα, it modulates transcription of these genes upon TNFα induction. This effect was obviously correlated with the amount of p65 binding to the promoter of these genes and with histone H3 acetylation and HDAC-3 removal. Conclusion While IE63 only affected transcription of a small number of cellular genes, it interfered with the TNF-inducibility of several NF-κB dependent genes by the accelerated resynthesis of the inhibitor IκBα. |
نوع الوثيقة: | article in journal/newspaper |
اللغة: | English |
تدمد: | 1471-2199 |
العلاقة: | http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17971236Test; urn:issn:1471-2199; https://orbi.uliege.be/handle/2268/1114Test; info:hdl:2268/1114; https://orbi.uliege.be/bitstream/2268/1114/1/Habran%202007.pdfTest; scopus-id:2-s2.0-37849011331; info:pmid:17971236 |
DOI: | 10.1186/1471-2199-8-99 |
الإتاحة: | https://doi.org/10.1186/1471-2199-8-99Test https://orbi.uliege.be/handle/2268/1114Test https://orbi.uliege.be/bitstream/2268/1114/1/Habran%202007.pdfTest |
حقوق: | open access ; http://purl.org/coar/access_right/c_abf2Test ; info:eu-repo/semantics/openAccess |
رقم الانضمام: | edsbas.FEB798C4 |
قاعدة البيانات: | BASE |
تدمد: | 14712199 |
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DOI: | 10.1186/1471-2199-8-99 |