Inhibits cell growth by regulating the TOR signaling pathway upstream of the TSC1-TSC2 complex and downstream of AKT1. Promotes neuronal cell death. Up-regulated in fibroblasts upon ionizing radiation, via a TP53-dependent pathway. Up-regulated by TP63 in primary keratinocytes, and down-regulated during keratinocyte differentiation. Up-regulated upon DNA alkylation. Up-regulated by amyloid beta-peptide and retinoic acid. Up-regulated by hypoxia, via a PI3K and HIF1A-dependent but TP53/TP63-independent mechanism. Broadly expressed, with lowest levels in brain, skeletal muscle and intestine. Up-regulated in substantia nigra neurons from Parkinson disease patients. Belongs to the DDIT4 family. Note: This description may include information from UniProtKB.
Biological Process: brain development; cell proliferation; defense response to virus; DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; gene expression; negative regulation of glycolysis; negative regulation of peptidyl-serine phosphorylation; negative regulation of TOR signaling pathway; nerve growth factor receptor signaling pathway; neuron differentiation; neuron migration; protein complex disassembly; response to hypoxia; transcription initiation from RNA polymerase II promoter
Alt. Names/Synonyms: DDIT4; Dig2; DNA damage-inducible transcript 4 protein; DNA-damage-inducible transcript 4; FLJ20500; HIF-1 responsive protein RTP801; HIF-1 responsive RTP801 (RTP801); Protein regulated in development and DNA damage response 1; REDD-1; REDD1; RP11-442H21.1; RTP801
LTP: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.