Anti-Forkhead box protein O1 FOXO1 Antibody

FOXO1, also known as FKHR or ForkHead in Rhabdomyosarcoma, is a 70 kDa protein which is a ubiquitously expressed member of a subfamily of the forkhead homeotic gene family of transcription factors and shuttles between the cytoplasm and nucleus. FOXO transcription factors are key players of cell fate decisions, metabolism, stress resistance, tumor suppression and are regulated by growth factors, oxidative stress or nutrient deprivation. In insulin-responsive tissues, stress or nutrient abundance triggers phosphorylation by PKB/AKT, blocking nuclear translocation and activity. Genetic mutations involving FOXO1A are a cause of alveolar rhabdomyosarcoma (RMS2) . Recent studies link the anti-tumor activity of FOXO1 and the process of autophagy.

FOXO1 antibody was raised against a 15 amino acid synthetic peptide near the amino terminus of human FOXO1. The immunogen is located within the first 50 amino acids of FOXO1.

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 (By similarity) .