期刊
MOLECULAR BIOLOGY OF THE CELL
卷 21, 期 23, 页码 4264-4274出版社
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E10-08-0705
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资金
- National Institutes of Health (NIH) [R01CA70896, R01CA75503, R01CA86072]
- NIH Cancer Center [P30CA56036]
- Dr. Ralph and Marian C. Falk Medical Research Trust
- Pennsylvania Department of Health
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.
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