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| Content Provider | Springer Nature Link |
|---|---|
| Author | So, Alex Yick Lun Fuente, Erwin Walter, Peter Shuman, Marc Bernales, Sebastián |
| Copyright Year | 2009 |
| Abstract | Accumulation of misfolded proteins in the endoplasmic reticulum (ER) induces the unfolded protein response (UPR). The UPR promotes cell survival by adjusting ER protein folding capacity but if homeostasis cannot be re-established, apoptosis is induced. The execution of life/death decisions is regulated by the three UPR branches (IRE1, PERK, ATF6) and their downstream effectors. Events that offset the balance of the UPR branches can have devastating consequences, and UPR misregulation has been correlated with various diseases, including metabolic and neurodegenerative diseases and cancer. In cancer, upregulation of the UPR is thought to provide a growth advantage to tumor cells. In contrast to this prevailing view, we report here an analysis of data obtained by others indicating that all three UPR branches appear selectively down-regulated in mouse models of prostate tumorigenesis. |
| Starting Page | 219 |
| Ending Page | 223 |
| Page Count | 5 |
| File Format | |
| ISSN | 01677659 |
| Journal | Cancer and Metastasis Reviews |
| Volume Number | 28 |
| Issue Number | 1-2 |
| e-ISSN | 15737233 |
| Language | English |
| Publisher | Springer US |
| Publisher Date | 2009-01-27 |
| Publisher Place | Boston |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Prostate cancer Tumorigenesis Unfolded protein response (UPR) IRE1 PERK ATF6 Biomedicine general Oncology Cancer Research |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cancer Research Oncology |
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