Anti-FOXO1 / Forkhead box protein O1, clone FOXO1/9792

0.2 mg/ml in 1X PBS with 0.1 mg/ml BSA (US sourced), 0.05% sodium azide. FKHR (for forkhead in rhabdomyosarcoma) and FKHRL1 are members of the forkhead family of transcription factors. Transcriptional activation of FKHR proteins is regulated by the serine/threonine kinase Akt1, which phosphorylates FKHRL1 and results in FKHRL1 associating with 14-3-3 proteins and being retained in the cytoplasm. Induction of apoptosis or withdrawal of growth factors stimulates dephosphorylation and nuclear translocation of FKHR proteins, leading to FKHR-induced gene-specific transcriptional activation. FKHR, also designated forkhead box protein O1A (FOXO1), is a ubiquitously expressed protein that shuttles between the cytoplasm and nucleus. Genetic mutations in FKHR genes, including the t(2,13) and t(1,3) translocations, are commonly found in alveolar rhabdomyosarcomas. These translocations result in the fusion of the amino terminus of Pax-3 or Pax-7, including the paired box and homeodomain DNA-binding domains, with the carboxyterminus of FKHR, which contains a transcriptional activation domain. The Pax-3/FKHR fusion protein appears to function as an oncogenic transcription factor that enhances the activation of normal Pax-3 target genes. Protein function: Transcription factor that is the main target of insulin signaling and regulates metabolic homeostasis in response to oxidative stress (PubMed:10358076, PubMed:12228231, PubMed:15220471, PubMed:15890677, PubMed:18356527, PubMed:19221179, PubMed:20543840, PubMed:21245099). 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' (PubMed:10358076). Activity suppressed by insulin (PubMed:10358076). Main regulator of redox balance and osteoblast numbers and controls bone mass. Orchestrates the endocrine function of the skeleton in regulating glucose metabolism. Also acts as a key regulator of chondrogenic commitment of skeletal progenitor cells in response to lipid availability: when lipids levels are low, translocates to the nucleus and promotes expression of SOX9, which induces chondrogenic commitment and suppresses fatty acid oxidation. 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. Acts as an inhibitor of glucose sensing in pancreatic beta cells by acting as a transcription repressor and suppressing expression of PDX1. In hepatocytes, promotes gluconeogenesis by acting together with PPARGC1A and CEBPA to activate the expression of genes such as IGFBP1, G6PC1 and PCK1. Also promotes gluconeogenesis by directly promoting expression of PPARGC1A and G6PC1 (PubMed:17024043). Important regulator of cell death acting downstream of CDK1, PKB/AKT1 and STK4/MST1 (PubMed:18356527, PubMed:19221179). Promotes neural cell death (PubMed:18356527). 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 (PubMed:20543840). Mediates the function of MLIP in cardiomyocytes hypertrophy and cardiac remodeling. Positive regulator of apoptosis in cardiac smooth muscle cells as a result of its transcriptional activation of pro-apoptotic genes (PubMed:19483080). Regulates endothelial cell (EC) viability and apoptosis in a PPIA/CYPA- dependent manner via transcription of CCL2 and BCL2L11 which are involved in EC chemotaxis and apoptosis (PubMed:31063815). [The UniProt Consortium]