ArticleMolecular and cellular biology1997
The viral oncoprotein E1A blocks transforming growth factor beta-mediated induction of p21/WAF1/Cip1 and p15/INK4B.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 96 citations in OpenAlex.
- Interleukin 4 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Viruses as key modulators of the TGF-β pathway; a double-edged sword involved in cancer.Reviews in medical virology · 2018Review
- Platelet activating factor-induced expression of p21 is correlated with histone acetylation.Scientific reports · 2017Article
- Phosphorylation: Implications in Cancer.The protein journal · 2017Review
- Zinc finger protein 451 is a novel Smad corepressor in transforming growth factor-β signaling.The Journal of biological chemistry · 2014Article
- Adenovirus E1A and E1B-19K proteins protect human hepatoma cells from transforming growth factor beta1-induced apoptosis.Virus research · 2010Article
- Association of v-ErbA with Smad4 disrupts TGF-beta signaling.Molecular biology of the cell · 2009Article
- Differential activation of ERK and Rac mediates the proliferative and anti-proliferative effects of hyaluronan and CD44.The Journal of biological chemistry · 2008Article
- Review
- p21WAF1/CIP1 selectively controls the transcriptional activity of estrogen receptor alpha.Molecular and cellular biology · 2005Article
- Article
- Epstein-Barr virus nuclear antigen 3C regulates cyclin A/p27 complexes and enhances cyclin A-dependent kinase activity.Journal of virology · 2004Article
- Transforming growth factor beta1 receptor II is downregulated by E1A in adenovirus-infected cells.Journal of virology · 2003Article
- Transforming growth factor beta 1 dysregulation in a human oral carcinoma tumour progression model.Cell proliferation · 2002Article
- The cytotoxic effect of E1B 55-kDa mutant adenovirus on human hepatocellular carcinoma cell lines.Cancer gene therapy · 2001Article
- Strategies in subversion: de-regulation of the mammalian cell cycle by viral gene products.International journal of experimental pathology · 2001Review
- Smad2, Smad3 and Smad4 cooperate with Sp1 to induce p15(Ink4B) transcription in response to TGF-beta.The EMBO journal · 2000Article
- A role for transcriptional repression of p21CIP1 by c-Myc in overcoming transforming growth factor beta -induced cell-cycle arrest.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The adenovirus early gene product E1A is a potent stimulator of cellular proliferation, which when overexpressed can overcome the growth-inhibitory effects of the polypeptide hormone transforming growth factor beta (TGF-beta). The ability of TGF-beta to arrest cell growth in G1 correlates with the transcriptional induction of the cyclin-dependent kinase inhibitors, p15/INK4B and p21/WAF1/Cip1; an inhibition of the G1 cyclin-Cdk complexes; and a maintenance of the retinoblastoma susceptibility gene product, Rb, in a hypophosphorylated state. The ability of E1A to overcome TGF-beta-mediated growth inhibition derives, in part, from its ability to sequester Rb and Rb family members. We report here that E1A also acts upstream of Rb by blocking the TGF-beta-mediated induction of p15 and p21. Consistent with these findings, E1A expression also blocks the ability of TGF-beta to inhibit Cdk2 kinase activity, as well as its ability to hold Rb in a hypophosphorylated state. The effect of E1A on the induction of p15 and p21 is independent of E1A's Rb binding activity. The E1A-mediated decrease in p15 levels is primarily the result of a block at the level of transcriptional activation by TGF-beta. This effect is dependent on E1A's ability to bind p300, one of E1A's target proteins. Thus, the ability of E1A to affect p15 and p21 expression represents an additional possible mechanism by which E1A can circumvent the negative regulation of cell cycle progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.