ArticleMolecular and cellular biology1992
Interaction of a common factor with ATF, Sp1, or TATAA promoter elements is required for these sequences to mediate transactivation by the adenoviral oncogene E1a.
Article in Molecular and cellular biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- A novel application of E1A in combination therapy with EGFR-TKI treatment in breast cancer.Oncotarget · 2016Article
- Nerve Growth factor regulation of cyclin D1 in PC12 cells through a p21RAS extracellular signal-regulated kinase pathway requires cooperative interactions between Sp1 and nuclear factor-kappaB.Molecular biology of the cell · 2008Article
- CREB (cAMP response element binding protein) and C/EBPalpha (CCAAT/enhancer binding protein) are required for the superstimulation of phosphoenolpyruvate carboxykinase gene transcription by adenoviral E1a and cAMP.The Biochemical journal · 2000Article
- Article
- Functional domains of the human orphan receptor ARP-1/COUP-TFII involved in active repression and transrepression.Molecular and cellular biology · 1997Article
- The Rb family contains a conserved cyclin-dependent-kinase-regulated transcriptional repressor motif.Molecular and cellular biology · 1996Article
- Domains A and B in the Rb pocket interact to form a transcriptional repressor motif.Molecular and cellular biology · 1996Article
- Transcription factor TFIID is a direct functional target of the adenovirus E1A transcription-repression domain.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Modulation of transcriptional activation of the proliferating cell nuclear antigen promoter by the adenovirus E1A 243-residue oncoprotein depends on proximal activators.Molecular and cellular biology · 1994Article
- Vascular cell adhesion molecule 1: contrasting transcriptional control mechanisms in muscle and endothelium.Proceedings of the National Academy of Sciences of the United States of America · 1993Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The adenovirus protein E1a stimulates transcription of both viral and cellular genes. Unlike most other transcription factors, it induces transactivation through several different promoter elements. The mechanism by which elements of diverse sequence mediate the effect of E1a is the focus of this study. Three E1a-responsive elements (an ATF site, an Sp1 site, and a TATA box containing the sequence TATAA) were studied to determine whether their interaction with a common factor is necessary for transactivation. In transfection assays, each element was used as a competitor against promoter constructs containing the other elements. The elements as competitors had no effect on basal transcription, but each competitor completely inhibited transactivation by E1a. Competitors that were not E1a responsive failed to inhibit transactivation. Therefore, either E1a itself or an E1a-inducible factor interacts with each of the elements to cause transactivation, most likely though an association with each element's specific binding protein.
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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.