Anti-FOXO1

FOXO1,also named as FOXO1A,FKHR and FKH1,is a member of the FOXO subfamily of Forkhead transcription factors. FOXO1 is a transcription factor which acts as a regulator of cell responses to oxidative stress. FOXO1 interacts with LRPPRC and SIRT1. In the presence of KIRT1,FOXO1 mediates down-regulation of cyclin D1 and up-regulation of CDKN1B levels which are required for cell transition from proliferative growth to quiescence. FOXO1 contains three predicted protein kinase B phosphorylation sites (Thr-24,Ser-256,and Ser-319) that are conserved in other FOXO proteins. The t(2,13) and the variant t(1,13) translocations generate PAX3/FKHR and PAX7/FKHR fusion proteins respectively. The resulting protein is a transcriptional activator. Defects in FOXO1 are a cause of rhabdomyosarcoma type 2 (RMS2). Protein function: Transcription factor that is the main target of insulin signaling and regulates metabolic homeostasis in response to oxidative stress. Binds to the insulin response element (IRE) with consensus sequence 5'-TT[G/A]TTTTG-3' and the related Daf-16 family binding element (DBE) with consensus sequence 5'- TT[G/A]TTTAC-3'. Activity suppressed by insulin. Main regulator of redox balance and osteoblast numbers and controls bone mass. Orchestrates the endocrine function of the skeleton in regulating glucose metabolism. Acts synergistically with ATF4 to suppress osteocalcin/BGLAP activity, increasing glucose levels and triggering glucose intolerance and insulin insensitivity. Also suppresses the transcriptional activity of RUNX2, an upstream activator of osteocalcin/BGLAP. In hepatocytes, promotes gluconeogenesis by acting together with PPARGC1A and CEBPA to activate the expression of genes such as IGFBP1, G6PC and PCK1. Important regulator of cell death acting downstream of CDK1, PKB/AKT1 and STK4/MST1. Promotes neural cell death. Mediates insulin action on adipose tissue. Regulates the expression of adipogenic genes such as PPARG during preadipocyte differentiation and, adipocyte size and adipose tissue-specific gene expression in response to excessive calorie intake. Regulates the transcriptional activity of GADD45A and repair of nitric oxide- damaged DNA in beta-cells. Required for the autophagic cell death induction in response to starvation or oxidative stress in a transcription-independent manner. Mediates the function of MLIP in cardiomyocytes hypertrophy and cardiac remodeling. [The UniProt Consortium]