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Papers In Press, published online ahead of print May 30, 2002
Institute for Medical Radiation and Cell Research, Wuerzburg 97078
Corresponding Author: rappur{at}mail.uni-wuerzburg.de
The c-Jun N-terminal kinases (JNKs) (also known as stress-activated protein kinases 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 pointed to a role of 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 SAPKb-MKK7 hybrid protein and using this constitutively active SAPKb we are able to demonstrate the transforming potential of activated JNK, which is weaker than that of classical oncogenes such as Ras or Raf. Inducible expression of SAPKb-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, expression of activated SAPKb resulted in the degradation 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.
J. Biol. Chem, 10.1074/jbc.M203010200
Submitted on March 28, 2002
Revised on May 29, 2002
Accepted on May 30, 2002
Constitutive JNK activation in NIH 3T3 fibroblasts induces a partially transformed phenotype
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