Anti-FOXO1 (Clone: ABM4E66) FITC Conjugated

FOXO1 is one of the fox proteins playing pivotal roles in several human intracellular pathways. These proteins are transcription factors acting as nuclear regulator of transcriptional activity of a number of metabolic processes such as the cellular response to oxidative stress. FOXO1 protein response to oxidative stress may be linked to Alzheimer's disease (AD) by means of insulin brain resistance. FOXO1 plays a critical role in establishing and maintaining the B cell specific differentiation program, but it is also responsible for cell death due to an inappropriate BCR signaling. This protein is highly expressed in B cells, is downregulated in Hodgkin and Reed-Sternberg (HRS) cells of cHL (Classical Hodgkin Lymphoma). 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 SKT4/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]