Literature DB >> 8206684

Endogenous TGF-beta contributes to the induction of the EBV lytic cycle in two Burkitt lymphoma cell lines.

L di Renzo1, A Altiok, G Klein, E Klein.   

Abstract

A low proportion of cells in the BL lines P3HR-I and Akata enter spontaneously into the EBV lytic cycle, detectable by the expression of early antigens (EA). We found that both lines produce the active and inactive forms of TGF beta. It was shown earlier that a larger number of cells can be induced to enter the lytic cycle by exposing P3HR-I to phorbol esters and n-butyrate and the surface IgG-positive Akata cells to anti-IgG. We now show that the same treatments raise the level of active TGF beta release. Exposure to anti-TGF beta antibodies reduced EA induction by 75-85%. Our results indicate that induction of the viral productive cycle by the above-mentioned reagents is at least partly dependent on the activation of endogenous TGF beta production.

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Year:  1994        PMID: 8206684     DOI: 10.1002/ijc.2910570623

Source DB:  PubMed          Journal:  Int J Cancer        ISSN: 0020-7136            Impact factor:   7.396


  23 in total

1.  Elevated serum transforming growth factor beta1 levels in Epstein-Barr virus-associated diseases and their correlation with virus-specific immunoglobulin A (IgA) and IgM.

Authors:  J Xu; A Ahmad; J F Jones; R Dolcetti; E Vaccher; U Prasad; J Menezes
Journal:  J Virol       Date:  2000-03       Impact factor: 5.103

2.  Activation of the BRLF1 promoter and lytic cycle of Epstein-Barr virus by histone acetylation.

Authors:  L K Chang; S T Liu
Journal:  Nucleic Acids Res       Date:  2000-10-15       Impact factor: 16.971

3.  Promoter sequences required for reactivation of Epstein-Barr virus from latency.

Authors:  Ulrich K Binné; Wolfgang Amon; Paul J Farrell
Journal:  J Virol       Date:  2002-10       Impact factor: 5.103

4.  Fusion of Epstein-Barr virus with epithelial cells can be triggered by αvβ5 in addition to αvβ6 and αvβ8, and integrin binding triggers a conformational change in glycoproteins gHgL.

Authors:  Liudmila S Chesnokova; Lindsey M Hutt-Fletcher
Journal:  J Virol       Date:  2011-09-28       Impact factor: 5.103

5.  Contribution of C/EBP proteins to Epstein-Barr virus lytic gene expression and replication in epithelial cells.

Authors:  Jian Huang; Gangling Liao; Honglin Chen; Frederick Y Wu; Lindsey Hutt-Fletcher; Gary S Hayward; S Diane Hayward
Journal:  J Virol       Date:  2006-02       Impact factor: 5.103

6.  Fusion of epithelial cells by Epstein-Barr virus proteins is triggered by binding of viral glycoproteins gHgL to integrins alphavbeta6 or alphavbeta8.

Authors:  Liudmila S Chesnokova; Stephen L Nishimura; Lindsey M Hutt-Fletcher
Journal:  Proc Natl Acad Sci U S A       Date:  2009-11-17       Impact factor: 11.205

7.  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

Review 8.  Regulation of the latent-lytic switch in Epstein-Barr virus.

Authors:  Shannon C Kenney; Janet E Mertz
Journal:  Semin Cancer Biol       Date:  2014-01-20       Impact factor: 15.707

9.  Activators of the Epstein-Barr virus lytic program concomitantly induce apoptosis, but lytic gene expression protects from cell death.

Authors:  G J Inman; U K Binné; G A Parker; P J Farrell; M J Allday
Journal:  J Virol       Date:  2001-03       Impact factor: 5.103

10.  Signal Transduction and Transcription Factor Modification during Reactivation of Epstein-Barr Virus from Latency.

Authors:  Helen Bryant; Paul J Farrell
Journal:  J Virol       Date:  2002-10       Impact factor: 5.103

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