CG&D
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Min, S.
Right arrow Articles by Taparowsky, E. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Min, S.
Right arrow Articles by Taparowsky, E. J.

Cell Growth & Differentiation, Vol 5, Issue 6 563-573, Copyright © 1994 by American Association of Cancer Research


ARTICLES

The transcription activation domains of v-Myc and VP16 interact with common factors required for cellular transformation and proliferation

S Min, SJ Crider-Miller and EJ Taparowsky
Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-1392.

The amino terminus of the avian myelocytomatosis virus MC29 v-Myc oncoprotein contains sequences that are essential for cellular transformation (S. Farina, et al. J. Virol., 66: 2698-2708, 1992; S. Min and E. J. Taparowsky. Oncogene, 7:1531-1540, 1992) and for the ability to activate gene transcription (S. Min and E. J. Taparowsky. Oncogene, 7:1531-1540, 1992). To investigate the molecular interactions that mediate these v-Myc-associated activities, we performed competition assays in which various regions of the v-Myc amino terminal transcription activation domain (TAD) were examined for their ability to inhibit transcription activation by v-Myc, VP16, and the myogenic regulatory factor MyoD. Overexpression of these transcriptional activators also was used to investigate whether Myc-interacting proteins were required for cellular transformation and cell proliferation events. Our results demonstrate that at least two distinct cellular activities interact with the v-Myc TAD and that it is the synergism between these activities that is required for v-Myc to function fully as a transcriptional activator. In addition, v-Myc activators squelch VP16- and MyoD-dependent transcription activation, suggesting that the v-Myc TAD interacts with a component of the general transcription machinery. In support of this observation, we found that overexpression of the v-Myc TAD inhibits ras-mediated cellular transformation as well as cell proliferation, underscoring the critical role these amino terminal Myc-interacting factors play in regulating the physiology of both normal and transformed cells.


This article has been cited by other articles:


Home page
Cancer Res.Home page
M. J. Gough, A. A. Melcher, A. Ahmed, M. R. Crittenden, D. S. Riddle, E. Linardakis, A. N. Ruchatz, L. M. Emiliusen, and R. G. Vile
Macrophages Orchestrate the Immune Response to Tumor Cell Death
Cancer Res., October 1, 2001; 61(19): 7240 - 7247.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
G. Foos, J. J. Garcia-Ramirez, C. K. Galang, and C. A. Hauser
Elevated Expression of Ets2 or Distinct Portions of Ets2 Can Reverse Ras-mediated Cellular Transformation
J. Biol. Chem., July 24, 1998; 273(30): 18871 - 18880.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cell Growth & Differentiation
Copyright © 1994 by the American Association of Cancer Research.