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 Schuur, E. R.
Right arrow Articles by Vogt, P. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schuur, E. R.
Right arrow Articles by Vogt, P. K.

Cell Growth & Differentiation, Vol 4, Issue 9 761-768, Copyright © 1993 by American Association of Cancer Research


ARTICLES

Chimeras of herpes simplex viral VP16 and jun are oncogenic

ER Schuur, EJ Parker and PK Vogt
Department of Microbiology, University of Southern California School of Medicine, Los Angeles.

The Jun protein binds DNA and regulates transcription as a component of the AP-1 transcription factor complex. In its oncogenic form, Jun can transform cells in culture and cause tumors in animals. Both trans-activation and transformation require several functional domains of Jun, including an amino-terminal trans-activation domain. In this study, properties of Jun required for trans-activation and transformation were explored by replacing the trans-activation domains of c-Jun and its oncogenic counterpart, v-Jun, with the constitutively active trans-activation domain from the herpes simplex virus VP16 protein. The VP16-v-Jun chimera retained similar oncogenic properties to its parent, v-Jun. The VP16-c-Jun chimera, however, was considerably more oncogenic than c-Jun. Substitutions of a phenylalanine in the VP16 domain of the VP16-c-Jun chimera diminished or abolished transformation. Each of the chimeras bound to the AP-1 consensus recognition sequence from the collagenase promoter or from the human T-cell leukemia virus type I long terminal repeat in vitro. None of the VP16-Jun chimeras efficiently stimulated transcription from the collagenase promoter or an artificial promoter containing the human T-cell leukemia virus type I element in vivo. These results demonstrate that the Jun trans-activation domain can be replaced by a heterologous trans-activation domain with retention of oncogenic activity. However, this oncogenic activity is not reflected in the trans-activating properties of the chimeras.


This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
S.-l. Fu, I. Bottoli, M. Goller, and P. K. Vogt
Heparin-binding epidermal growth factor-like growth factor, a v-Jun target gene, induces oncogenic transformation
PNAS, May 11, 1999; 96(10): 5716 - 5721.
[Abstract] [Full Text] [PDF]


Home page
Mol. Cell. Biol.Home page
S. Huguier, J. Baguet, S. Perez, H. van Dam, and M. Castellazzi
Transcription Factor ATF2 Cooperates with v-Jun To Promote Growth Factor-Independent Proliferation In Vitro and Tumor Formation In Vivo
Mol. Cell. Biol., December 1, 1998; 18(12): 7020 - 7029.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
U. Kruse, J. S. Iacovoni, M. E. Goller, and P. K. Vogt
Hormone-regulatable neoplastic transformation induced by a Jun-estrogen receptor chimera
PNAS, November 11, 1997; 94(23): 12396 - 12400.
[Abstract] [Full Text] [PDF]


Home page
J Biol ChemHome page
E. R. Schuur, G. A. Henderson, L. A. Kmetec, J. D. Miller, H. G. Lamparski, and D. R. Henderson
Prostate-specific Antigen Expression Is Regulated by an Upstream Enhancer
J. Biol. Chem., March 22, 1996; 271(12): 7043 - 7051.
[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 © 1993 by the American Association of Cancer Research.