The transcription activation domains of v-Myc and VP16 interact with common factors required for cellular transformation and proliferation.
Cell Growth Differ
; 5(6): 563-73, 1994 Jun.
Article
em En
| MEDLINE
| ID: mdl-8086335
ABSTRACT
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, 71531-1540, 1992) and for the ability to activate gene transcription (S. Min and E. J. Taparowsky. Oncogene, 71531-1540, 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.
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Base de dados:
MEDLINE
Assunto principal:
Fatores de Transcrição
/
Proteínas Oncogênicas Virais
/
Proteína Oncogênica p55(v-myc)
/
Proteína Vmw65 do Vírus do Herpes Simples
/
Proteína MyoD
Limite:
Animals
Idioma:
En
Revista:
Cell Growth Differ
Assunto da revista:
BIOLOGIA MOLECULAR
Ano de publicação:
1994
Tipo de documento:
Article