| First Author | Sandow JJ | Year | 2014 |
| Journal | Cell Death Differ | Volume | 21 |
| Issue | 3 | Pages | 475-80 |
| PubMed ID | 24292555 | Mgi Jnum | J:229151 |
| Mgi Id | MGI:5750859 | Doi | 10.1038/cdd.2013.168 |
| Citation | Sandow JJ, et al. (2014) ER stress does not cause upregulation and activation of caspase-2 to initiate apoptosis. Cell Death Differ 21(3):475-80 |
| abstractText | A recent report claimed that endoplasmic reticulum (ER) stress activates the ER trans-membrane receptor IRE1alpha, leading to increased caspase-2 levels via degradation of microRNAs, and consequently induction of apoptosis. This observation casts caspase-2 into a central role in the apoptosis triggered by ER stress. We have used multiple cell types from caspase-2-deficient mice to test this hypothesis but failed to find significant impact of loss of caspase-2 on ER-stress-induced apoptosis. Moreover, we did not observe increased expression of caspase-2 protein in response to ER stress. Our data strongly argue against a critical role for caspase-2 in ER-stress-induced apoptosis. |
