ArticleMolecular and cellular biology2003
HMG-I(Y) and the CBP/p300 coactivator are essential for human papillomavirus type 18 enhanceosome transcriptional activity.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 36 citations in OpenAlex.
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- Integrating quantitative proteomics with accurate genome profiling of transcription factors by greenCUT&RUN.Nucleic acids research · 2021Article
- Epigenetic regulation of human papillomavirus transcription in the productive virus life cycle.Seminars in immunopathology · 2020Review
- Dynamics of sequestering the limiting p300/CBP, viral cis-regulatory elements, and disease.Journal of biosciences · 2020Review
- A systems biology analysis of the changes in gene expression via silencing of HPV-18 E1 expression in HeLa cells.Open biology · 2014Article
- HMGA proteins as modulators of chromatin structure during transcriptional activation.Frontiers in cell and developmental biology · 2014Review
- Binding site specificity and factor redundancy in activator protein-1-driven human papillomavirus chromatin-dependent transcription.The Journal of biological chemistry · 2011Article
- The E2F5 repressor is an activator of E6/E7 transcription and of the S-phase entry in HPV18-associated cells.Oncogene · 2010Article
- Optimal transactivation by Epstein-Barr nuclear antigen 1 requires the UR1 and ATH1 domains.Journal of virology · 2009Article
- Human papilloma virus-dependent HMGA1 expression is a relevant step in cervical carcinogenesis.Neoplasia (New York, N.Y.) · 2008Article
- The E6 protein of the cutaneous human papillomavirus type 8 can stimulate the viral early and late promoters by distinct mechanisms.Journal of virology · 2006Article
- HIV-1 clade promoters strongly influence spatial and temporal dynamics of viral replication in vivo.The Journal of clinical investigation · 2005Article
- Dominant-negative c-Jun (TAM67) target genes: HMGA1 is required for tumor promoter-induced transformation.Oncogene · 2004Article
- Papillomavirus interaction with cellular chromatin.Biochimica et biophysica actaReview
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Authors and funding
4 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
A strong epithelial specific enhancer drives transcription of the human papillomavirus type 18 (HPV18) oncogenes. Its activity depends on the formation of a higher-order nucleoprotein complex (enhanceosome) involving the sequence-specific JunB/Fra2 transcription factor and the HMG-I(Y) architectural protein. Here we show that proteins from HeLa cell nuclear extract cover almost all of the HPV18 enhancer sequences and that it contains seven binding sites for the purified HMG-I(Y) protein, providing evidence for a tight nucleoprotein structure. Binding of HMG-I(Y) and the AP1 heterodimer from HeLa nuclear extract to overlapping sites of the core enhanceosome is cooperative. The integrity of this specific HMG-I(Y) binding site is as essential as the AP1 binding site for the enhancer function, indicating the fundamental role played by this architectural protein. We demonstrate that the CBP/p300 coactivator is recruited by the HPV18 enhanceosome and that it is limiting for transcriptional activation, since it is sequestered by the adenovirus E1A protein and by the JunB/Fra2 positive factor in excess. We show the involvement of JunB and p300 in vivo in the HPV18 transcription by chromatin immunoprecipitation of HPV18 sequences in HeLa cells.
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