Anti-FOXO1 Rabbit antibody

Anti-FOXO1 Rabbit antibody

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• Material Safety Data Sheets (MSDS)

FOXO1 Rabbit polyclonal antibody

WB, IHC-P, ICC/IF, FC

Human, Mouse, Rat

FKH 1;FKH1;FKH1;FKHR;FKHR;Forkhead (Drosophila) homolog 1 (rhabdomyosarcoma);Forkhead (Drosophila) homolog 1 (rhabdomyosarcoma);Forkhead box O1;Forkhead box protein O1; Forkhead box protein O1A;Forkhead in rhabdomyosarcoma;Forkhead antibody; Drosophila antibody; homolog of antibody

Rabbit IgG

Antigen: A synthetic peptide of human FOXO1A

Polyclonal

Supplied in 50nM Tris-Glycine(pH 7.4), 0.15M Nacl, 40%Glycerol, 0.01% sodium azide and 0.05% BSA.

Store at -20°C. Stable for 12 months from date of receipt.

Swiss-Prot Acc.Q12778.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 .