NDLI: E1A-dependent trans-activation of the c-fos promoter requires the TATAA sequence.

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E1A-dependent trans-activation of the c-fos promoter requires the TATAA sequence.

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E1A-dependent trans-activation of the c-fos promoter requires the TATAA sequence.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Simon, M. C. Heintz, N. Nevins, J. R. Rooney, R. J. Fisch, T. M.
Description	Author Affiliation: Simon MC ( Howard Hughes Medical Institute, Rockefeller University, New York, NY 10021.);
Abstract	Previous experiments have demonstrated that transcription of the human c-fos oncogene is activated through the action of the 289-amino acid adenovirus E1A gene product. In this study we have utilized a series of c-fos promoter deletion and substitution mutants to define regulatory sequences that allow the induction by E1A. Although the deletion of upstream promoter sequences has varying degrees of effect on overall promoter activity, these deletions retain inducibility by E1A. This includes the deletion of the serum response element and two elements that bind the ATF transcription factor. In fact, a c-fos promoter deleted to position -53, which leaves the TATA element but no other known functional element, retains inducibility, indicating a role for the TATA element in E1A control. Indeed, substitution of the c-fos TATA element (TATAA) with a TATA sequence from the simian virus 40 early promoter (TATTTAT) abolishes E1A inducibility; this promoter does retain responsiveness to cAMP induction, however, demonstrating that this TATTTAT substitution is functional. We conclude that the E1A-dependent activation of c-fos transcription is mediated through an effect on a TATA-binding protein that has specificity for the TATAA sequence.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	2
Volume Number	87
Language	English
Publisher	National Academy of Sciences
Publisher Date	1990-03-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Adenoviruses, Human Genetics DNA-Binding Proteins Oncogene Proteins, Viral Promoter Regions, Genetic Protein-Tyrosine Kinases Proto-Oncogene Proteins Proto-Oncogenes Transcriptional Activation Adenovirus Early Proteins Animals HeLa Cells Molecular Sequence Data Oligonucleotide Probes Plasmids Proto-Oncogene Proteins C-fos Regulatory Sequences, Nucleic Acid Vero Cells Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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