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Perspectives
JNK2: A Negative Regulator of Cellular Proliferation
Kanaga Sabapathy and Erwin F.Wagner
volume 3 | issue 12
december 2004Pages: 1520 - 1523
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The three different c-Jun N-terminal kinases (JNKs) are activated in multiple cell types by both apoptotic and mitogenic signals, and in turn regulate the activity of transcription factors such as c-Jun. Being highly homologous and ubiquitously expressed, the JNK1 and JNK2 proteins have been thought to perform redundant functions in many physiological process. However, our data from Jnk1-/- or Jnk2-/- cells and mice suggest that both JNK isozymes perform distinct functions in regulating cellular proliferation via differential regulation of c-Jun, which is a critical regulator of cell-cycle progression. Absence of JNK1, the positive regulator of c-Jun, leads to decreased fibroblast proliferation. In contrast, JNK2 deficiency leads to reduced c-Jun degradation, thereby augmenting c-Jun levels and cellular proliferation. Various cell types including fibroblasts, erythroblasts and hepatocytes from Jnk2-/- mice exhibit increased proliferation rates compared to their wild-type counterparts. These data therefore suggests that JNK2, in contrast to JNK1, is a negative regulator of cellular proliferation in multiple cell types.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.