| First Author | Yamazaki T | Year | 2010 |
| Journal | Biochem Biophys Res Commun | Volume | 392 |
| Issue | 2 | Pages | 196-200 |
| PubMed ID | 20060811 | Mgi Jnum | J:157864 |
| Mgi Id | MGI:4437179 | Doi | 10.1016/j.bbrc.2010.01.013 |
| Citation | Yamazaki T, et al. (2010) Facilitation of DNA damage-induced apoptosis by endoplasmic reticulum protein mitsugumin23. Biochem Biophys Res Commun 392(2):196-200 |
| abstractText | The endoplasmic reticulum (ER) emanates context-dependent signals, thereby mediating cellular response to a variety of stresses. However, the underlying molecular mechanisms have been enigmatic. To better understand the signaling capacity of the ER, we focused on roles played by mitsugumin23 (MG23), a protein residing predominantly in this organelle. Overexpression of MG23 in human embryonic kidney 293T cells specifically enhanced apoptosis triggered by etoposide, a DNA-damaging anti-cancer drug. Conversely, genetic deletion of MG23 reduced susceptibility of thymocytes to DNA damage-induced apoptosis, which was demonstrated by whole-body irradiation experiments. In this setting, induction of the tumor-suppressor gene p53 was attenuated in MG23-knockout thymocytes as compared with their wild-type counterparts, consistent with the elevated radioresistance. It is therefore suggested that MG23 is an essential component of ER-generated lethal signals provoked upon DNA damage, specifying cell fate under pathophysiological conditions. |
