Literature DB >> 12438580

The Epstein-Barr virus immediate-early protein BZLF1 induces expression of E2F-1 and other proteins involved in cell cycle progression in primary keratinocytes and gastric carcinoma cells.

Amy Mauser1, Elizabeth Holley-Guthrie, Adam Zanation, Wendall Yarborough, William Kaufmann, Aloysius Klingelhutz, William T Seaman, Shannon Kenney.   

Abstract

The Epstein-Barr virus (EBV) immediate-early protein BZLF1 mediates the switch between the latent and lytic forms of EBV infection and has been previously shown to induce a G(1)/S block in cell cycle progression in some cell types. To examine the effect of BZLF1 on cellular gene expression, we performed microarray analysis on telomerase-immortalized human keratinocytes that were mock infected or infected with a control adenovirus vector (AdLacZ) or a vector expressing the EBV BZLF1 protein (AdBZLF1). Cellular genes activated by BZLF1 expression included E2F-1, cyclin E, Cdc25A, and a number of other genes involved in cell cycle progression. Immunoblot analysis confirmed that BZLF1 induced expression of E2F-1, cyclin E, Cdc25A, and stem loop binding protein (a protein known to be primarily expressed during S phase) in telomerase-immortalized keratinocytes. Similarly, BZLF1 increased expression of E2F-1, cyclin E, and stem loop binding protein (SLBP) in primary tonsil keratinocytes. In contrast, BZLF1 did not induce E2F-1 expression in normal human fibroblasts. Cell cycle analysis revealed that while BZLF1 dramatically blocked G(1)/S progression in normal human fibroblasts, it did not significantly affect cell cycle progression in primary human tonsil keratinocytes. Furthermore, in EBV-infected gastric carcinoma cells, the BZLF1-positive cells had an increased number of cells in S phase compared to the BZLF1-negative cells. Thus, in certain cell types (but not others), BZLF1 enhances expression of cellular proteins associated with cell cycle progression, which suggests that an S-phase-like environment may be advantageous for efficient lytic EBV replication in some cell types.

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Year:  2002        PMID: 12438580      PMCID: PMC136734          DOI: 10.1128/jvi.76.24.12543-12552.2002

Source DB:  PubMed          Journal:  J Virol        ISSN: 0022-538X            Impact factor:   5.103


  80 in total

1.  The Epstein-Barr virus bZIP transcription factor Zta causes G0/G1 cell cycle arrest through induction of cyclin-dependent kinase inhibitors.

Authors:  C Cayrol; E K Flemington
Journal:  EMBO J       Date:  1996-06-03       Impact factor: 11.598

2.  G0/G1 growth arrest mediated by a region encompassing the basic leucine zipper (bZIP) domain of the Epstein-Barr virus transactivator Zta.

Authors:  C Cayrol; E Flemington
Journal:  J Biol Chem       Date:  1996-12-13       Impact factor: 5.157

3.  trans activation of the latent Epstein-Barr virus (EBV) genome after transfection of the EBV DNA fragment.

Authors:  K Takada; N Shimizu; S Sakuma; Y Ono
Journal:  J Virol       Date:  1986-03       Impact factor: 5.103

4.  Epstein-Barr virus exploits the normal cell pathway to regulate Rb activity during the immortalisation of primary B-cells.

Authors:  E J Cannell; P J Farrell; A J Sinclair
Journal:  Oncogene       Date:  1996-10-03       Impact factor: 9.867

5.  The human cytomegalovirus IE1-72 protein interacts with the cellular p107 protein and relieves p107-mediated transcriptional repression of an E2F-responsive promoter.

Authors:  E E Poma; T F Kowalik; L Zhu; J H Sinclair; E S Huang
Journal:  J Virol       Date:  1996-11       Impact factor: 5.103

6.  Human cytomegalovirus inhibits cellular DNA synthesis and arrests productively infected cells in late G1.

Authors:  W A Bresnahan; I Boldogh; E A Thompson; T Albrecht
Journal:  Virology       Date:  1996-10-01       Impact factor: 3.616

7.  Cytomegalovirus infection induces high levels of cyclins, phosphorylated Rb, and p53, leading to cell cycle arrest.

Authors:  F M Jault; J M Jault; F Ruchti; E A Fortunato; C Clark; J Corbeil; D D Richman; D H Spector
Journal:  J Virol       Date:  1995-11       Impact factor: 5.103

8.  Epstein-Barr viral latency is disrupted by the immediate-early BRLF1 protein through a cell-specific mechanism.

Authors:  S Zalani; E Holley-Guthrie; S Kenney
Journal:  Proc Natl Acad Sci U S A       Date:  1996-08-20       Impact factor: 11.205

9.  A second site for Epstein-Barr virus shedding: the uterine cervix.

Authors:  J W Sixbey; S M Lemon; J S Pagano
Journal:  Lancet       Date:  1986-11-15       Impact factor: 79.321

10.  Both Epstein-Barr virus (EBV)-encoded trans-acting factors, EB1 and EB2, are required to activate transcription from an EBV early promoter.

Authors:  A Chevallier-Greco; E Manet; P Chavrier; C Mosnier; J Daillie; A Sergeant
Journal:  EMBO J       Date:  1986-12-01       Impact factor: 11.598

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  26 in total

1.  Inhibition of S-phase cyclin-dependent kinase activity blocks expression of Epstein-Barr virus immediate-early and early genes, preventing viral lytic replication.

Authors:  Ayumi Kudoh; Tohru Daikoku; Yutaka Sugaya; Hiroki Isomura; Masatoshi Fujita; Tohru Kiyono; Yukihiro Nishiyama; Tatsuya Tsurumi
Journal:  J Virol       Date:  2004-01       Impact factor: 5.103

2.  Mutation of a single amino acid residue in the basic region of the Epstein-Barr virus (EBV) lytic cycle switch protein Zta (BZLF1) prevents reactivation of EBV from latency.

Authors:  Celine Schelcher; Sarah Valencia; Henri-Jacques Delecluse; Matthew Hicks; Alison J Sinclair
Journal:  J Virol       Date:  2005-11       Impact factor: 5.103

3.  The Epstein-Barr virus replication protein BBLF2/3 provides an origin-tethering function through interaction with the zinc finger DNA binding protein ZBRK1 and the KAP-1 corepressor.

Authors:  Gangling Liao; Jian Huang; Elizabeth D Fixman; S Diane Hayward
Journal:  J Virol       Date:  2005-01       Impact factor: 5.103

4.  Epstein-Barr virus BZLF1 protein binds to mitotic chromosomes.

Authors:  Amy L Adamson
Journal:  J Virol       Date:  2005-06       Impact factor: 5.103

5.  Epstein-Barr virus BGLF4 kinase induces premature chromosome condensation through activation of condensin and topoisomerase II.

Authors:  Chung-Pei Lee; Jen-Yang Chen; Jiin-Tarng Wang; Keiji Kimura; Ai Takemoto; Chih-Chung Lu; Mei-Ru Chen
Journal:  J Virol       Date:  2007-03-14       Impact factor: 5.103

6.  AP-1 homolog BZLF1 of Epstein-Barr virus has two essential functions dependent on the epigenetic state of the viral genome.

Authors:  Markus Kalla; Anne Schmeinck; Martin Bergbauer; Dagmar Pich; Wolfgang Hammerschmidt
Journal:  Proc Natl Acad Sci U S A       Date:  2009-12-22       Impact factor: 11.205

7.  Epstein-Barr virus BZLF1 protein impairs accumulation of host DNA damage proteins at damage sites in response to DNA damage.

Authors:  Jie Yang; Wen Deng; Pok M Hau; Jia Liu; Victoria M Y Lau; Annie L M Cheung; Michael S Y Huen; Sai W Tsao
Journal:  Lab Invest       Date:  2015-06-01       Impact factor: 5.662

8.  BGLF4 kinase modulates the structure and transport preference of the nuclear pore complex to facilitate nuclear import of Epstein-Barr virus lytic proteins.

Authors:  Chou-Wei Chang; Chung-Pei Lee; Mei-Tzu Su; Ching-Hwa Tsai; Mei-Ru Chen
Journal:  J Virol       Date:  2014-11-19       Impact factor: 5.103

9.  Kaposi's sarcoma-associated herpesvirus K-bZIP represses gene transcription via SUMO modification.

Authors:  Yoshihiro Izumiya; Thomas J Ellison; Edward T H Yeh; Jae U Jung; Paul A Luciw; Hsing-Jien Kung
Journal:  J Virol       Date:  2005-08       Impact factor: 5.103

10.  The BRRF1 early gene of Epstein-Barr virus encodes a transcription factor that enhances induction of lytic infection by BRLF1.

Authors:  Gregory K Hong; Henri-Jacques Delecluse; Henri Gruffat; Thomas E Morrison; Wen-Hai Feng; Alain Sergeant; Shannon C Kenney
Journal:  J Virol       Date:  2004-05       Impact factor: 5.103

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