c-Jun NH2-terminal kinase (JNK) 1 and JNK2 have been assumed to complement each other and mediate the same or similar biological functions. However, our recent reports indicated that 7,12-dimethylbenz(a)anthracene/12-O-tetradecanoylphorbol-13-acetate-induced tumor development is suppressed in Jnk2 knockout mice but enhanced in Jnk1 knockout mice. In the present work, primary embryo cells were isolated from wild-type, Jnk1-/- and Jnk2-/- mice and used for cDNA microarray analysis. The patterns of gene expression in Jnk1-/-, Jnk2-/-, and wild-type cells are different. After 12-O-tetradecanoylphorbol-13-acetate treatment, the changes in the gene expression profiles in three different kinds of cells appear to agree with the differences in susceptibility to tumori-genesis of each respective animal model. These results suggest that JNK1 and JNK2 proteins have different roles in modulating cell function.
|Original language||English (US)|
|Number of pages||5|
|State||Published - Mar 1 2002|