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Publication : A HIF-1 target, ATIA, protects cells from apoptosis by modulating the mitochondrial thioredoxin, TRX2.

First Author  Choksi S Year  2011
Journal  Mol Cell Volume  42
Issue  5 Pages  597-609
PubMed ID  21658601 Mgi Jnum  J:173568
Mgi Id  MGI:5014460 Doi  10.1016/j.molcel.2011.03.030
Citation  Choksi S, et al. (2011) A HIF-1 Target, ATIA, Protects Cells from Apoptosis by Modulating the Mitochondrial Thioredoxin, TRX2. Mol Cell 42(5):597-609
abstractText  The regulation of apoptosis is critical for controlling tissue homeostasis and preventing tumor formation and growth. Reactive oxygen species (ROS) generation plays a key role in such regulation. Here, we describe a HIF-1 target, Vasn/ATIA (anti-TNFalpha-induced apoptosis), which protects cells against TNFalpha- and hypoxia-induced apoptosis. Through the generation of ATIA knockout mice, we show that ATIA protects cells from apoptosis through regulating the function of the mitochondrial antioxidant, thioredoxin-2, and ROS generation. ATIA is highly expressed in human glioblastoma, and ATIA knockdown in glioblastoma cells renders them sensitive to hypoxia-induced apoptosis. Therefore, ATIA is not only a HIF-1 target that regulates mitochondrial redox pathways but also a potentially diagnostic marker and therapeutic target in human glioblastoma.
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