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Epstein-Barr Nuclear Antigen 1 modulates replication of oriP-plasmids by impeding replication and transcription fork migration through the family of repeats

By Ashok Aiyar, Siddhesh Aras, Amber Washington, Gyanendra Singh and Ronald B Luftig
Topics: Research
Publisher: BioMed Central
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Provided by: PubMed Central

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  1. (1987). Replication of latent Epstein-Barr virus genomes in Raji cells.
  2. (1991). Epstein-Barr virus-derived plasmids replicate only once per cell cycle and are not amplified after entry into cells.
  3. (1985). AJ: Mapping genetic elements of Epstein-Barr virus that facilitate extrachromosomal persistence of Epstein-Barr virus-derived plasmids in human cells. Mol Cell Biol
  4. (1985). Stable replication of plasmids derived from Epstein-Barr virus in various mammalian cells. Nature
  5. (1990). SD: Definition of the sequence requirements for binding of the EBNA-1 protein to its palindromic target sites in EpsteinBarr virus DNA.
  6. (1985). GS: Sequence-specific DNA binding of the Epstein-Barr virus nuclear antigen (EBNA-1) to clustered sites in the plasmid maintenance region. Cell
  7. (2001). Yates JL: Human DNA replication initiation factors, ORC and MCM, associate with oriP of Epstein-Barr virus. P r o c N a t l A c a d S c i U S A
  8. (2001). A: Replication from oriP of EpsteinBarr virus requires human ORC and is inhibited by geminin. Cell
  9. (2001). Human origin recognition complex binds to the region of the latent origin of DNA replication of Epstein-Barr virus.
  10. (2008). Lieberman PM: RNA-dependent recruitment of the origin recognition complex.
  11. (1998). The plasmid replicon of EBV consists of multiple cis-acting elements that facilitate DNA synthesis by the cell and a viral maintenance element.
  12. (1989). Calos MP: Isolation of human sequences that replicate autonomously in human cells. Mol Cell Biol
  13. (1991). SD: Functional domains of Epstein-Barr virus nuclear antigen EBNA-1. J Virol
  14. (1996). AM: Crystal structure of the DNA-binding domain of the Epstein-Barr virus origin-binding protein, EBNA1, bound to DNA. Cell
  15. (1983). Two Epstein-Barr viral nuclear neoantigens distinguished by gene transfer, serology, and chromosome binding. Proc Natl Acad Sci USA
  16. (1999). JC: Mapping EBNA-1 domains involved in binding to metaphase chromosomes.
  17. (2003). Aiyar A: Metaphase chromosome tethering is necessary for the DNA synthesis and maintenance of oriP plasmids but is insufficient for transcription activation by Epstein-Barr nuclear antigen 1. J Virol
  18. (2004). Aiyar A: The amino terminus of Epstein-Barr Virus (EBV) nuclear antigen 1 contains AT hooks that facilitate the replication and partitioning of latent EBV genomes by tethering them to cellular chromosomes.
  19. (2001). E: Maintenance of Epstein-Barr virus (EBV) oriP-based episomes requires EBV-encoded nuclear antigen-1 chromosome-binding domains, which can be replaced by high-mobility group-I or histone H1. Proc Natl Acad Sci USA
  20. (1998). Stability without a centromere. Proc Natl Acad Sci USA
  21. (2007). The coupling of synthesis and partitioning of EBV's plasmid replicon is revealed in live cells.
  22. (1989). Schildkraut CL: The Epstein-Barr virus origin of plasmid replication, oriP, contains both the initiation and termination sites of DNA replication. Cell
  23. (1996). Schildkraut CL: Role of the EBNA-1 protein in pausing of replication forks in the Epstein-Barr virus genome.
  24. (2003). Aiyar A: The spacing between adjacent binding sites in the family of repeats affects the functions of Epstein-Barr nuclear antigen 1 in transcription activation and stable plasmid maintenance. Virology
  25. (2001). The cis-acting family of repeats can inhibit as well as stimulate establishment of an oriP replicon.
  26. (1989). Molecular Cloning: A Laboratory Manual 2nd edition.
  27. (1998). Fusions between Epstein-Barr viral nuclear antigen-1 of Epstein-Barr virus and the large T-antigen of simian virus 40 replicate their cognate origins.
  28. (1997). Sugden B: Dominant-negative inhibitors of EBNA-1 of Epstein-Barr virus.
  29. (1977). Characteristics of a human cell line transformed by DNA from human adenovirus type 5. J Gen Virol
  30. (1967). Selective extraction of polyoma DNA from infected mouse cell cultures.
  31. (1999). Laimins LA: DNA replication of human papillomavirus type 31 is modulated by elements of the upstream regulatory region that lie 5' of the minimal origin.
  32. (1975). Detection of specific sequences among DNA fragments separated by gel electrophoresis.
  33. (1987). Subramani S: Firefly luciferase gene: structure and expression in mammalian cells. Mol Cell Biol
  34. (1984). DNA sequence and expression of the B95-8 Epstein-Barr virus genome. Nature
  35. (1994). Calos MP: Transcription inhibits the replication of autonomously replicating plasmids in human cells.
  36. (2007). Dissection of mammalian replicators by a novel plasmid stability assay.
  37. (1995). Alberts BM: Head-on collision between a DNA replication apparatus and RNA polymerase transcription complex. Science
  38. (2005). Sap1p binds to Ter1 at the ribosomal DNA of Schizosaccharomyces pombe and causes polar replication fork arrest.
  39. (2004). D: swi1- and swi3-dependent and independent replication fork arrest at the ribosomal DNA of Schizosaccharomyces pombe.
  40. (1996). Newlon CS: DNA replication fork pause sites dependent on transcription. Science
  41. (2007). Takeda S: Cooperative roles of vertebrate Fbh1 and Blm DNA helicases in avoidance of crossovers during recombination initiated by replication fork collapse. Mol Cell Biol
  42. (1987). GN: Two major replicating simian virus 40 chromosome classes. Synchronous replication fork movement is associated with bound large T antigen during elongation.
  43. (1988). Simian virus 40 large T antigen DNA helicase. Characterization of the ATPasedependent DNA unwinding activity and its substrate requirements.
  44. (2001). Schildkraut CL: Visualization of DNA replication on individual Epstein-Barr virus episomes. Science
  45. (2004). Schildkraut CL: Plasticity of DNA replication initiation in Epstein-Barr virus episomes. PLoS Biol
  46. (1995). Schildkraut CL: Initiation of latent DNA replication in the Epstein-Barr virus genome can occur at sites other than the genetically defined origin. Mol Cell Biol
  47. (2008). Identifying a property of origins of DNA synthesis required to support plasmids stably in human cells.
  48. (2006). Deregulated replication licensing causes DNA fragmentation consistent with head-to-tail fork collision. Mol Cell
  49. (1996). GM: Sensitivity and selectivity of the DNA damage sensor responsible for activating p53-dependent G1 arrest.
  50. (2007). GG: NBS1 mediates ATR-dependent RPA hyperphosphorylation following replication-fork stall and collapse.
  51. (2002). Fork reversal and ssDNA accumulation at stalled replication forks owing to checkpoint defects. Science
  52. (1995). Grummt I: Molecular coevolution of mammalian ribosomal gene terminator sequences and the transcription termination factor TTF-I.
  53. (1992). Grummt I: Limited proteolysis unmasks specific DNA-binding of the murine RNA polymerase I-specific transcription termination factor TTFI.
  54. (1989). MD: Epstein-Barr virus small RNA (EBER) genes: unique transcription units that combine RNA polymerase II and III promoter elements. Cell
  55. (1993). MD: Upstream basal promoter element important for exclusive RNA polymerase
  56. (1995). An EBNA-1-dependent enhancer acts from a distance of 10 kilobase pairs to increase expression of the Epstein-Barr virus LMP gene.
  57. (1996). SH: oriP is essential for EBNA gene promoter activity in Epstein-Barr virus-immortalized lymphoblastoid cell lines.
  58. (1986). B: trans activation of an Epstein-Barr viral transcriptional enhancer by the Epstein-Barr viral nuclear antigen 1. Mol Cell Biol
  59. (2006). Transcriptional activation by EBV nuclear antigen 1 is essential for the expression of EBV's transforming genes. Proc Natl Acad Sci USA
  60. (1989). JL: Multiple EBNA1-binding sites are required to form an EBNA1-dependent enhancer and to activate a minimal replicative origin within oriP of EpsteinBarr virus.

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