Anti-DDIT4

REDD-1, also designated DNA-damage-inducible transcript 4, dig2 or RTP801, is thought to function in the regulation of reactive oxygen species (ROS). REDD-1 expression has also been linked to apoptosis, Ab toxicity and the pathogenesis of ischemic diseases. As an HIF-1-responsive gene, REDD-1 exhibits strong hypoxia-dependent upregulation in ischemic cells of neuronal origin. In response to stress due to DNA damage and glucocorticoid treatment, REDD-1 is upregulated at the transcriptional level. REDD-1 negatively regulates the mammalian target of Rapamycin (mTOR), a serine/threonine kinase often referred to as FRAP. It is crucial in the coupling of extra- and intracellular cues to FRAP regulation. The absence of REDD-1 is associated with the development of retinopathy, a major cause of blindness. Protein function: Regulates cell growth, proliferation and survival via inhibition of the activity of the mammalian target of rapamycin complex 1 (mTORC1). Inhibition of mTORC1 is mediated by a pathway that involves DDIT4/REDD1, AKT1, the TSC1-TSC2 complex and the GTPase RHEB. Plays an important role in responses to cellular energy levels and cellular stress, including responses to hypoxia and DNA damage. Regulates p53/TP53-mediated apoptosis in response to DNA damage via its effect on mTORC1 activity. Its role in the response to hypoxia depends on the cell type, it mediates mTORC1 inhibition in fibroblasts and thymocytes, but not in hepatocytes. Required for mTORC1-mediated defense against viral protein synthesis and virus replication. Inhibits neuronal differentiation and neurite outgrowth mediated by NGF via its effect on mTORC1 activity. Required for normal neuron migration during embryonic brain development. Plays a role in neuronal cell death. [The UniProt Consortium]