ArticleJournal of virology1995
The N-terminal region of the adenovirus type 5 E1A proteins can repress expression of cellular genes via two distinct but overlapping domains.
Article in Journal of virology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- A cancer-specific transcriptional signature in human neoplasia.The Journal of clinical investigation · 2005Article
- The MN1 oncoprotein synergizes with coactivators RAC3 and p300 in RAR-RXR-mediated transcription.Oncogene · 2003Article
- Article
- A specific lysine in c-Jun is required for transcriptional repression by E1A and is acetylated by p300.The EMBO journal · 2001Article
- The N-terminal transactivation domain of ATF2 is a target for the co-operative activation of the c-jun promoter by p300 and 12S E1A.Oncogene · 1999Article
- A novel function of adenovirus E1A is required to overcome growth arrest by the CDK2 inhibitor p27(Kip1).The EMBO journal · 1998Article
- Identification of specific amino acid residues of adenovirus 12 E1A involved in transformation and p300 binding.Virus genes · 1997Article
- Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Repression of cyclin D1 expression does not contribute to initiation or maintenance of cell transformation by adenovirus type 5 E1.Journal of virology · 1996Article
- A novel E1A domain mediates skeletal-muscle-specific enhancer repression independently of pRB and p300 binding.Molecular and cellular biology · 1996Article
- Adenovirus E1A downregulates cJun- and JunB-mediated transcription by targeting their coactivator p300.Molecular and cellular biology · 1996Article
- Induction of susceptibility to tumor necrosis factor by E1A is dependent on binding to either p300 or p105-Rb and induction of DNA synthesis.Journal of virology · 1996Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
The transforming E1A 12S and E1A 13S proteins of human adenovirus type 5 (Ad5) contain two and three conserved regions, respectively. In the present study, the contribution of sequences in the nonconserved N-terminal region of the E1A proteins to morphological transformation and to down-regulation of a number of mitogen-inducible genes was investigated. As described previously, transformation of NRK cells (an established normal rat kidney cell line) results in denser cell growth and a cuboidal cellular morphology. None of the cells expressing N-terminally mutated E1A proteins, however, show these transformed properties, which suggests an important role for sequences in that domain. The decrease in cyclin D1 levels requires exactly the same sequences. The ability to transform NRK cells and to reduce cyclin D1 levels does not correlate with the presence in the E1A proteins of binding domains for p300, CBP, p107, pRb, cyclin A, or cdk2. In contrast, down-regulation of expression of the JE gene in NRK cells and repression of transcription of the collagenase gene in human HeLa cells does correlate with the presence in the E1A proteins of an intact binding domain for p300 and CBP. The results suggest that the N-terminal domain of the E1A proteins can repress expression of cellular genes by at least two different mechanisms.
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