| First Author | Yim HY | Year | 2012 |
| Journal | Biochem Biophys Res Commun | Volume | 423 |
| Issue | 2 | Pages | 436-40 |
| PubMed ID | 22683641 | Mgi Jnum | J:185351 |
| Mgi Id | MGI:5428346 | Doi | 10.1016/j.bbrc.2012.05.154 |
| Citation | Yim HY, et al. (2012) The mitochondrial pathway and reactive oxygen species are critical contributors to interferon-alpha/beta-mediated apoptosis in Ubp43-deficient hematopoietic cells. Biochem Biophys Res Commun 423(2):436-40 |
| abstractText | UBP43 (also known as USP18) plays a role in the negative regulation of interferon-alpha/beta signaling, and bone marrow cells in Ubp43-deficient mice exhibited hypersensitivity to interferon-alpha/beta-mediated apoptosis. Here, we show that the mitochondrial apoptotic pathway and reactive oxygen species are major contributors to the elevated interferon-alpha/beta-mediated apoptosis in Ubp43-deficient mouse bone marrow cells and in UBP43-knockdown THP-1 cells. Furthermore, TRAIL and FASL, which were proposed as apoptosis inducers upon interferon-alpha/beta treatment in UBP43-knockdown adherent cancer cells, did not cause apoptosis in these hematopoietic cells. Therefore, although UBP43 depletion can cause hypersensitivity to interferon-alpha/beta-mediated apoptosis in a broad range of cell types, the downstream pathway may vary depending on the cell type. |
