ArticleJournal of virology2000
A role for SKIP in EBNA2 activation of CBF1-repressed promoters.
Article in Journal of virology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
54 citing papers in PubMed, 110 citations in OpenAlex.
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- Novel replisome-associated proteins at cellular replication forks in EBV-transformed B lymphocytes.PLoS pathogens · 2019Article
- Species-specific functions of Epstein-Barr virus nuclear antigen 2 (EBNA2) reveal dual roles for initiation and maintenance of B cell immortalization.PLoS pathogens · 2017Article
- BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2.PLoS pathogens · 2016Article
- Epstein-Barr Virus: Diseases Linked to Infection and Transformation.Frontiers in microbiology · 2016Review
- Expression and prognostic role of SKIP in human breast carcinoma.Journal of molecular histology · 2014Article
- Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Analyzing the nuclear complexes of Notch signaling by electrophoretic mobility shift assay.Methods in molecular biology (Clifton, N.J.) · 2014Article
- Impact of EBV essential nuclear protein EBNA-3C on B-cell proliferation and apoptosis.Future microbiology · 2013Review
- The nuclear chaperone nucleophosmin escorts an Epstein-Barr Virus nuclear antigen to establish transcriptional cascades for latent infection in human B cells.PLoS pathogens · 2012Article
- Structural and functional analysis of the repressor complex in the Notch signaling pathway of Drosophila melanogaster.Molecular biology of the cell · 2011Article
- C-terminal region of EBNA-2 determines the superior transforming ability of type 1 Epstein-Barr virus by enhanced gene regulation of LMP-1 and CXCR7.PLoS pathogens · 2011Article
- EBV nuclear antigen EBNALP dismisses transcription repressors NCoR and RBPJ from enhancers and EBNA2 increases NCoR-deficient RBPJ DNA binding.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Article
- Xenopus skip modulates Wnt/beta-catenin signaling and functions in neural crest induction.The Journal of biological chemistry · 2010Article
- LIM domain only 4 protein promotes granulocyte colony-stimulating factor-induced signaling in neurons.Cellular and molecular life sciences : CMLS · 2010Article
- NKAP is a transcriptional repressor of notch signaling and is required for T cell development.Immunity · 2009Article
- Regulation of cyclin D1 RNA stability by SNIP1.Cancer research · 2008Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
EBNA2 is essential for Epstein-Barr virus (EBV) immortalization of B lymphocytes. EBNA2 functions as a transcriptional activator and targets responsive promoters through interaction with the cellular DNA binding protein CBF1. We have examined the mechanism whereby EBNA2 overcomes CBF1-mediated transcriptional repression. A yeast two-hybrid screen performed using CBF1 as the bait identified a protein, SKIP, which had not previously been recognized as a CBF1-associated protein. Protein-protein interaction assays demonstrated contacts between SKIP and the SMRT, CIR, Sin3A, and HDAC2 proteins of the CBF1 corepressor complex. Interestingly, EBNA2 also interacted with SKIP in glutathione S-transferase affinity and mammalian two-hybrid assays and colocalized with SKIP in immunofluorescence assays. Interaction with SKIP was not affected by mutation of EBNA2 conserved region 6, the CBF1 interaction region, but was abolished by mutation of conserved region 5. Mutation of conserved region 5 also severely impaired EBNA2 activation of a reporter containing CBF1 binding sites. Thus, interaction with both CBF1 and SKIP is necessary for efficient promoter activation by EBNA2. A model is presented in which EBNA2 competes with the SMRT-corepressor complex for contacts on SKIP and CBF1.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.