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Originally published In Press as doi:10.1074/jbc.M203010200 on May 30, 2002

J. Biol. Chem., Vol. 277, Issue 33, 29510-29518, August 16, 2002
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Constitutive JNK Activation in NIH 3T3 Fibroblasts Induces a Partially Transformed Phenotype*

Ulrike E. E. RennefahrtDagger , Bertram Illert§, Eugen KerkhoffDagger , Jakob TroppmairDagger , and Ulf R. RappDagger ||

From the Dagger  Institut für Medizinische Strahlenkunde und Zellforschung, Universität Würzburg, 97078 Würzburg, Germany and the § Chirurgische Klinik und Poliklinik, Universität Würzburg, 97080 Würzburg, Germany

The c-Jun N-terminal kinases (JNKs) (also known as stress-activated protein kinases or SAPKs), members of the mitogen-activated protein kinase (MAPK) family, regulate gene expression in response to a variety of physiological and unphysiological stimuli. Gene knockout experiments and the use of dominant interfering mutants have pointed to a role for JNKs in the processes of cell differentiation and survival as well as oncogenic transformation. Direct analysis of the transforming potential of JNKs has been hampered so far by the lack of constitutively active forms of these kinases. Recently, such mutants have become available by fusion of the MAPK with its direct upstream activator kinase. We have generated a constitutively active SAPKbeta -MKK7 hybrid protein and, using this constitutively active kinase, we are able to demonstrate the transforming potential of activated JNK, which is weaker than that of classical oncogenes such as Ras or Raf. The inducible expression of SAPKbeta -MKK7 caused morphological transformation of NIH 3T3 fibroblasts. Additionally, these cells formed small foci of transformed cells and grew anchorage-independent in soft agar. Furthermore, similar to oncogenic Ras and Raf, the expression of activated SAPKbeta resulted in the disassembly of F-actin stress fibers. Our data suggest that constitutive JNK activation elicits major aspects of cellular transformation but is unable to induce the complete set of changes which are required to establish the fully transformed phenotype.

* This work was supported by a grant from the Deutsche Forschungsgemeinschaft (special research fields 465 and 581) and by the Mildred Scheel Stiftung.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Shared senior authorship.

|| To whom correspondence should be addressed: Inst. für Medizinische Strahlenkunde und Zellforschnung (MSZ), Universität Würzburg, Versbacher Str. 5, 97078 Würzburg, Germany. Tel.: 49-931-201-45140; Fax: 49-931-201-45835; E-mail: rappur@mail.uni-wuerzburg.de.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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