Adenovirus E1A products suppress myogenic differentiation and inhibit transcription from muscle-specific promoters

@article{Webster1988AdenovirusEP,
  title={Adenovirus E1A products suppress myogenic differentiation and inhibit transcription from muscle-specific promoters},
  author={Keith A. Webster and George E. O. Muscat and Larry Kedes},
  journal={Nature},
  year={1988},
  volume={332},
  pages={553-557}
}
The primary function of the adenovirus ElA-region genes is to activate other adenoviral genes during a permissive viral infection by modifying the host cell transcriptional apparatus1,2. Host cell immortalization, or transformation by the whole adenoviral early region, presumably results as a consequence of these modifications. Both transcriptional activation and transcriptional repression of non-adenoviral genes by the E1A proteins have been reported3–9. It is currently not clear which, if… 

Characterisation of cellular and viral genes induced by the adenovirus E1A gene

Adenovirus infection was shown to increase expression of a polyubiquitin gene, Ub B, which could result in increased ubiquitin levels, leading to increased activity of an ATP dependent protein-degradation pathway,Which could rapidly degrade foreign virion components, resulting in an inhibition of the lyric cycle.

General repression of enhanson activity by the adenovirus-2 E1A proteins.

The results indicate that the amino-terminal region of the protein, which contains domain 1, plays a crucial role in repression, possibly by interfering in the transcriptional activation process at a step common to all trans-acting enhancer factors.

Transcriptional Coactivator p300 Stimulates Cell Type-specific Gene Expression in Cardiac Myocytes*

E1A’s transcriptional repression of celltype-specific genes in cardiac myocytes is mediated through its binding of p300 proteins, and these proteins appear to be involved in maintaining both cell type-specific gene expression and cell cycle arrest in cardiacMyocytes.

Adenovirus 5 E1A represses muscle-specific enhancers and inhibits expression of the myogenic regulatory factor genes, MyoD1 and myogenin.

It is concluded that adenovirus 5 E1A exerts a negative effect on the differentiation of skeletal muscle cells by interfering with the expression of myogenic regulatory factor genes that are essential for the transcriptional activation of the contractile protein gene set.

Adenovirus E1A Inhibits Cardiac Myocyte-specific Gene Expression through Its Amino Terminus*

It is concluded that cardiac-specific and general promoter inhibition by E1A occurs by distinct mechanisms and that heart-specific gene expression is modulated by cellular factors interacting with the E 1A p300/CBP-binding domain.

Expression of E1A in terminally differentiated muscle cells reactivates the cell cycle and suppresses tissue-specific genes by separable mechanisms

The results show that E1A reactivates the cell cycle and suppresses tissue-specific gene expression in terminally differentiated muscle cells, thus causing dedifferentiation.

Adenovirus 5 E 1 A Represses Muscle-specific Enhancers and Inhibits Expression of the Myogenic Regulatory Factor Genes , MyoDi and Myogenin ’

It is concluded that adenovirus 5 E1A exerts a negative effed on the differentiation of skeletal muscle cells by interfering with the expression of myogenic regulatory fador genes that are essential for the transcriptional adivation of the contradile protein gene set.

Inhibition of muscle differentiation by the adenovirus E1a protein: repression of the transcriptional activating function of the HLH protein Myf-5.

Evidence that E1a interferes with the expression of myogenin and the activity of Myf-5, the two myogenic helix-loop-helix (HLH) proteins that are expressed in L6 muscle cells is provided and it is demonstrated that the carboxy-terminal trans-activator domain and probably the basic-HLH region of My f-5 constitute targets for the inhibition by E1A.

The transcription-repression domain of the adenovirus E1A oncoprotein targets p300 at the promoter

Findings provide support for the hypothesis that p300 can serve as a scaffold for the E1A repression domain to access specific cellular gene promoters involved in growth regulation.

Adenovirus E1A Represses Cardiac Gene Transcription and Reactivates DNA Synthesis in Ventricular Myocytes, via Alternative Pocket Protein- and p300-binding Domains (*)

To examine the potential impact of disrupting “pocket” protein function on cardiac differentiation and growth, we introduced 12 S E1A genes into neonatal ventricular myocytes, by adenoviral gene
...

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