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| Content Provider | PubMed Central |
|---|---|
| Author | Isabel, Garcia-cao Lafuente, María José Criado, Luis M. Diaz Meco, María Teresa Serrano, Manuel Jorge, Moscat |
| Copyright Year | 2003 |
| Abstract | The Par4 gene was first identified in prostate cells undergoing apoptosis after androgen withdrawal. PAR4 was subsequently shown to interact with, and inhibit, atypical protein kinase C isoforms, functioning as a negative regulator of the NF-κB pathway. This may explain its pro-apoptotic function in overexpression experiments. To determine the physiological role of PAR4, we have derived primary embryonic fibroblasts (EFs) from Par4−/− mice. We show here that loss of PAR4 leads to a reduction in the ability of tumour necrosis factor-α (TNF-α) to induce apoptosis by increased activation of NF-κB. Consistent with recent reports demonstrating the antagonistic actions of NF-κB and c-Jun amino-terminal kinase (JNK) signalling, we have found that Par4−/− cells show a reduced activation of the sustained phase of JNK and p38 stimulation by TNF-α and interleukin 1. Higher levels of an anti-apoptotic JNK-inhibitor protein, X-chromosome-linked inhibitor of apoptosis, in Par4−/− EFs might explain the inhibition of JNK activation in these cells. |
| Related Links | http://dx.doi.org/10.1038/sj.embor.embor769 |
| Starting Page | 307 |
| File Format | |
| ISSN | 14693178 |
| e-ISSN | 14693178 |
| Journal | EMBO Reports |
| Issue Number | 3 |
| Volume Number | 4 |
| Language | English |
| Publisher Date | 2003-03-01 |
| Access Restriction | Open |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Genetics Biochemistry Molecular Biology |
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