| First Author | Katiyar S | Year | 2010 |
| Journal | Mol Biol Cell | Volume | 21 |
| Issue | 23 | Pages | 4264-74 |
| PubMed ID | 20926681 | Mgi Jnum | J:182934 |
| Mgi Id | MGI:5317097 | Doi | 10.1091/mbc.E10-08-0705 |
| Citation | Katiyar S, et al. (2010) C-jun inhibits mammary apoptosis in vivo. Mol Biol Cell 21(23):4264-74 |
| abstractText | c-jun, which is overexpressed in a number of human cancers encodes a critical component of the AP-1 complex. c-jun has been shown to either induce or inhibit cellular apoptosis. Germ line deletion of both c-jun alleles is embryonically lethal. To determine the role of the endogenous c-jun gene in apoptosis, we performed mammary epithelial cell-targeted somatic deletion using floxed c-jun (c-jun(f/f)) conditional knockout mice. Laser capture microdissection demonstrated endogenous c-jun inhibits expression of apoptosis inducing genes and reactive oxygen species (ROS)-reducing genes (MnSOD, catalase). ROS have been implicated in apoptosis and undergo enzymatic elimination via MnSOD and CuZnSOD with further detoxification via catalase. c-jun-mediated survival was in part dependent on ROS production. c-jun-mediated repression of MnSOD and catalase occurred via mitochondrial complex I and NOX I. Collectively, these studies define a pivotal role of endogenous c-jun in promoting cell survival via maintaining mitochondrial integrity and expression of the key regulators of ROS production. |
