| First Author | Ventura JJ | Year | 2003 |
| Journal | Mol Cell Biol | Volume | 23 |
| Issue | 8 | Pages | 2871-82 |
| PubMed ID | 12665585 | Mgi Jnum | J:82740 |
| Mgi Id | MGI:2654979 | Doi | 10.1128/MCB.23.8.2871-2882.2003 |
| Citation | Ventura JJ, et al. (2003) c-Jun NH(2)-terminal kinase is essential for the regulation of AP-1 by tumor necrosis factor. Mol Cell Biol 23(8):2871-82 |
| abstractText | The c-Jun NH(2)-terminal kinase (JNK) is activated by the cytokine tumor necrosis factor (TNF). This pathway is implicated in the regulation of AP-1-dependent gene expression by TNF. To examine the role of the JNK signaling pathway, we compared the effects of TNF on wild-type and Jnk1(-/-) Jnk2(-/-) murine embryo fibroblasts. We show that JNK is required for the normal regulation of AP-1 by TNF. The JNK-deficient cells exhibited decreased expression of c-Jun, JunD, c-Fos, Fra1, and Fra2; decreased phosphorylation of c-Jun and JunD; and decreased AP-1 DNA binding activity. The JNK-deficient cells also exhibited defects in the regulation of the AP-1-related transcription factor ATF2. These changes were associated with marked defects in TNF-regulated gene expression. The JNK signal transduction pathway is therefore essential for AP-1 transcription factor regulation in cells exposed to TNF. |
