Literature DB >> 10656694

Consequences of disruption of the interaction between p53 and the larger adenovirus early region 1B protein in adenovirus E1 transformed human cells.

F G Hutton1, A S Turnell, P H Gallimore, R J Grand.   

Abstract

The adenovirus early region 1B (Ad E1B) genes have no transforming capability of their own but markedly increase the transformation frequency of Ad E1A following co-transfection into mammalian cells. The larger E1B proteins of both Ad2/5 and Ad12 bind to p53 and inhibit its ability to transcriptionally activate other genes. We have previously demonstrated that synthetic peptides identical to the binding sites for p53 on both the Ad2 and Ad12 E1B proteins will disrupt the interaction in vivo and in vitro. In the work presented here we have examined the effects of complex dissociation on Ad E1-transformed human cells. It has been shown, using confocal microscopy, that when the peptide identical to the p53 binding site was added to Ad5 E1-transformed cells it initally located in the cytoplasmic dense bodies where it caused disruption of the p53/E1B complex. Peptide and p53 then translocated to the nucleus. In Ad12 E1-transformed cells the peptide localized in the nucleus directly and there caused a reorganization of p53 staining from a highly organized, 'flecked' distribution to one in which nuclear staining was homogeneous and diffuse. Peptides added to either Ad5 E1 or Ad12 E1 transformed cells resulted in the release of transcriptionally active p53. Interestingly, the level of p53 then fell presumably as a result of proteasomal action - this was probably a reflection of the short half-life of 'free' (i.e. dissociated) p53 compared to that of the bound protein. Free p53 did not cause apoptosis in target cells probably due to the presence of the smaller (19K) E1B proteins. However, addition of peptide leads to a significant reduction in cell growth rate. We have further demonstrated that a significant proportion of those cells which had taken up peptide had ceased DNA synthesis, probably due to a p53-induced cell cycle arrest. The role of the larger EIB protein during transformation is considered in view of these data.

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Year:  2000        PMID: 10656694     DOI: 10.1038/sj.onc.1203316

Source DB:  PubMed          Journal:  Oncogene        ISSN: 0950-9232            Impact factor:   9.867


  11 in total

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Authors:  C Endter; J Kzhyshkowska; R Stauber; T Dobner
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Authors:  B R Dix; S J Edwards; A W Braithwaite
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4.  Timely synthesis of the adenovirus type 5 E1B 55-kilodalton protein is required for efficient genome replication in normal human cells.

Authors:  Jasdave S Chahal; S J Flint
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5.  Serotype-specific inactivation of the cellular DNA damage response during adenovirus infection.

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6.  The adenoviral E1B 55-kilodalton protein controls expression of immune response genes but not p53-dependent transcription.

Authors:  Daniel L Miller; Brenden Rickards; Michael Mashiba; Wenying Huang; S J Flint
Journal:  J Virol       Date:  2009-02-11       Impact factor: 5.103

7.  Impact of the adenoviral E4 Orf3 protein on the activity and posttranslational modification of p53.

Authors:  Caroline J DeHart; David H Perlman; S J Flint
Journal:  J Virol       Date:  2015-01-07       Impact factor: 5.103

8.  Adenovirus E4orf3 targets transcriptional intermediary factor 1γ for proteasome-dependent degradation during infection.

Authors:  Natalie A Forrester; Rakesh N Patel; Thomas Speiseder; Peter Groitl; Garry G Sedgwick; Neil J Shimwell; Robert I Seed; Pól Ó Catnaigh; Christopher J McCabe; Grant S Stewart; Thomas Dobner; Roger J A Grand; Ashley Martin; Andrew S Turnell
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9.  Adenovirus type 5 early region 1B 156R protein promotes cell transformation independently of repression of p53-stimulated transcription.

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Journal:  J Virol       Date:  2006-10-18       Impact factor: 5.103

10.  In vivo potential effects of adenovirus type 5 E1A and E1B on lung carcinogenesis and lymphoproliferative inflammation.

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