Epigenetic reprogramming by Adenovirus E1A that causes transformations of the cell were discovered by Roberto Ferrari and his co-workers from the University of California (USA).

Adenovirus E1A wakes up dormant cells to activate replication. The scientists observed that E1A relocalised RB (retinoblastoma) proteins RB, p300 and p107 and p300/CBP histone acetyltransferases globally on promoters. Acetylation of histone H3 lysine-18 (H3K18) was restricted to a limited set of genes by this procedure, thereby stimulating cell cycling and inhibiting antiviral reactions and differentiation of the cells.

Shortly after expression, E1A temporarily binds to promoters of cell cycle- and proliferation-associated genes. Within the promoter context accumulation of p300/CBP, PCAF (p300/CBP-associated factor) occurs, at the same time H3K18. RB proteins are depleted and transcriptional activation take place.
The promoters of antiviral genes are also transient binding partners of E1A, augmenting RB, p300 and H4K16 (acetylated). The liaison also increases nucleosome density and transcriptional repression.

Lateron, E1A and p107 are bound mostly to promoters of genes orchestrating development and differentiation and repress transcription of these genes. For the correct temporal order of E1A binding, interactions with p300/CBP and RB proteins are essential hinting at pivotal effects of epigenetics in this context of cell transformation.

Related antibodies on antibodies-online.com:

Adenovirus E1A

RB (retinoblastoma) proteins

p107 (Retinoblastoma-like 1)

p300

CREB Binding Protein (CBP)

PCAF (P300/CBP-associated factor)

Histon H3, Lysin 18 acetylated

Histon H4, Lysin 16 acetylated

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