REDD1, also named as RTP801 and DDIT4, belongs to the DDIT4 family. REDD1 promotes neuronal cell death. It is a novel transcriptional target of p53 implicated ROS in the p53-dependent DNA damage response. REDD1 controlled cell growth under energy stress, as an essential regulator of TOR activity through the TSC1/2 complex. REDD-1 expression has also been linked to apoptosis, Aβ 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[PMID: 19996311]. In response to stress due to DNA damage and glucocorticoid treatment, REDD-1 is upregulated at the transcriptional level[PMID: 21733849]. REDD-1 negatively regulates the mammalian target of Rapamycin, a serine/threonine kinase often referred to as mTOR[PMID: 22951983]. It is crucial in the coupling of extra- and intracellular cues to mTOR regulation. The absence of REDD-1 is associated with the development of retinopathy, a major cause of blindness[PMID: 22304497]. REDD1 is a new host defense factor, and chemical activation of REDD1 expression represents a potent antiviral intervention strategy[PMID: 21909097]. REDD1 has a predicted molecular weight of 25kd. Because of multiple lysines in the proteins, REDD1 offen migrates around 35KD on Western blot[PMID: 19221489]. This antibody is a rabbit polyclonal antibody raised against full length human REDD1 antigen.