Adenovirus — Effect of Adenovirus E1A Oncogene on DNA Replication Dynamics
Citation(s)
Abbas T, Dutta A CRL4Cdt2: master coordinator of cell cycle progression and genome stability. Cell Cycle. 2011 Jan 15;10(2):241-9. Epub 2011 Jan 15. Review.
Abbas T, Shibata E, Park J, Jha S, Karnani N, Dutta A CRL4(Cdt2) regulates cell proliferation and histone gene expression by targeting PR-Set7/Set8 for degradation. Mol Cell. 2010 Oct 8;40(1):9-21. doi: 10.1016/j.molcel.2010.09.014.
Arias EE, Walter JC Strength in numbers: preventing rereplication via multiple mechanisms in eukaryotic cells. Genes Dev. 2007 Mar 1;21(5):497-518. Review.
Avvakumov N, Côté J Functions of myst family histone acetyltransferases and their link to disease. Subcell Biochem. 2007;41:295-317. Review.
Baluchamy S, Rajabi HN, Thimmapaya R, Navaraj A, Thimmapaya B Repression of c-Myc and inhibition of G1 exit in cells conditionally overexpressing p300 that is not dependent on its histone acetyltransferase activity. Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9524-9. Epub 2003 Jul 25.
Berk AJ Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus. Oncogene. 2005 Nov 21;24(52):7673-85. Review.
Breckenridge DG, Shore GC Regulation of apoptosis by E1A and Myc oncoproteins. Crit Rev Eukaryot Gene Expr. 2000;10(3-4):273-80. Review.
Brustel J, Tardat M, Kirsh O, Grimaud C, Julien E Coupling mitosis to DNA replication: the emerging role of the histone H4-lysine 20 methyltransferase PR-Set7. Trends Cell Biol. 2011 Aug;21(8):452-60. doi: 10.1016/j.tcb.2011.04.006. Epub 2011 May 31. Review.
DeCaprio JA How the Rb tumor suppressor structure and function was revealed by the study of Adenovirus and SV40. Virology. 2009 Feb 20;384(2):274-84. doi: 10.1016/j.virol.2008.12.010. Epub 2009 Jan 17. Review.
Deissler H, Opalka B Therapeutic transfer of DNA encoding adenoviral E1A. Recent Pat Anticancer Drug Discov. 2007 Jan;2(1):1-10. Review.
Goren A, Tabib A, Hecht M, Cedar H DNA replication timing of the human beta-globin domain is controlled by histone modification at the origin. Genes Dev. 2008 May 15;22(10):1319-24. doi: 10.1101/gad.468308. Epub 2008 Apr 28.
Kadeppagari RK, Sankar N, Thimmapaya B Adenovirus transforming protein E1A induces c-Myc in quiescent cells by a novel mechanism. J Virol. 2009 May;83(10):4810-22. doi: 10.1128/JVI.02145-08. Epub 2009 Mar 11.
Lavia P, Mileo AM, Giordano A, Paggi MG Emerging roles of DNA tumor viruses in cell proliferation: new insights into genomic instability. Oncogene. 2003 Sep 29;22(42):6508-16. Review.
Levine AJ The common mechanisms of transformation by the small DNA tumor viruses: The inactivation of tumor suppressor gene products: p53. Virology. 2009 Feb 20;384(2):285-93. doi: 10.1016/j.virol.2008.09.034. Epub 2008 Dec 11. Review.
Liao Y, Yu D, Hung MC Novel approaches for chemosensitization of breast cancer cells: the E1A story. Adv Exp Med Biol. 2007;608:144-69. Review.
Miotto B, Struhl K HBO1 histone acetylase activity is essential for DNA replication licensing and inhibited by Geminin. Mol Cell. 2010 Jan 15;37(1):57-66. doi: 10.1016/j.molcel.2009.12.012.
Miotto B, Struhl K HBO1 histone acetylase is a coactivator of the replication licensing factor Cdt1. Genes Dev. 2008 Oct 1;22(19):2633-8. doi: 10.1101/gad.1674108.
Moran E DNA tumor virus transforming proteins and the cell cycle. Curr Opin Genet Dev. 1993 Feb;3(1):63-70. Review.
Saksouk N, Avvakumov N, Côté J (de)MYSTification and INGenuity of tumor suppressors. Cell Mol Life Sci. 2008 Apr;65(7-8):1013-8. doi: 10.1007/s00018-008-7459-x. Review.
Sankar N, Kadeppagari RK, Thimmapaya B c-Myc-induced aberrant DNA synthesis and activation of DNA damage response in p300 knockdown cells. J Biol Chem. 2009 May 29;284(22):15193-205. doi: 10.1074/jbc.M900776200. Epub 2009 Mar 30.
Singhal G, Leo E, Setty SK, Pommier Y, Thimmapaya B Adenovirus E1A oncogene induces rereplication of cellular DNA and alters DNA replication dynamics. J Virol. 2013 Aug;87(15):8767-78. doi: 10.1128/JVI.00879-13. Epub 2013 Jun 5.
Interventional studies are often prospective and are specifically tailored to evaluate direct impacts of treatment or preventive measures on disease.
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Phase 3: The drug or treatment is given to large groups of people to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.
Phase 4: Studies are done after the drug or treatment has been marketed to gather information on the drug's effect in various populations and any side effects associated with long-term use.