|Application ||WB, IHC|
|Calculated MW||71277 Da|
|Other Names||Forkhead box protein O3, AF6q21 protein, Forkhead in rhabdomyosarcoma-like 1, FOXO3, FKHRL1, FOXO3A|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human FOXO3a was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||FOXO3a Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Transcriptional activator which triggers apoptosis in the absence of survival factors, including neuronal cell death upon oxidative stress (PubMed:10102273, PubMed:16751106). Recognizes and binds to the DNA sequence 5'-[AG]TAAA[TC]A-3' (PubMed:21329882). Participates in post-transcriptional regulation of MYC: following phosphorylation by MAPKAPK5, promotes induction of miR-34b and miR-34c expression, 2 post-transcriptional regulators of MYC that bind to the 3'UTR of MYC transcript and prevent its translation (PubMed:21329882). In response to metabolic stress, translocates into the mitochondria where it promotes mtDNA transcription (PubMed:23283301).|
|Cellular Location||Cytoplasm, cytosol. Nucleus. Mitochondrion matrix Mitochondrion outer membrane; Peripheral membrane protein; Cytoplasmic side. Note=Retention in the cytoplasm contributes to its inactivation (PubMed:10102273, PubMed:15084260, PubMed:16751106). Translocates to the nucleus upon oxidative stress and in the absence of survival factors (PubMed:10102273, PubMed:16751106). Translocates in a AMPK- dependent manner into the mitochondrion in response to metabolic stress (PubMed:23283301, PubMed:29445193)|
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Provided below are standard protocols that you may find useful for product applications.
Forkhead box O-class (FOXO) transcription factors are mammalian homologue of DAF-16, a known lifespan regulator of Caenorhabditis elegans. FOXO transcription factors, such as FOXO1, FOXO3a, and FOXO4, have been linked to the regulation of cell cycle, apoptosis, DNA repair, oxidative stress, and metabolism (1). FOXO proteins are proposed to be dual regulated by Akt-mediated phosphorylation and Skp2-mediated ubiquitination, which are usually initiated by growth factors and cytokines. FOXO proteins are also activated by stress, which induces gene expression that contributes to cell cycle arrest, implicating FOXO proteins as tumor suppressors (2). Specifically, FOXO3a (FKHR-L1) is a transcriptional activator for apoptosis in the absence of survival factors, such as in neural cell death triggered by oxidative stress. In the presence of survival factors like IGF-1, AKT1/PKB phosphorylates on Thr-32 and Ser-253. However, in the absence of survival factors, FOXO3a is dephospholyated and translocated to the nucleus inducing transcription of target genes and apoptosis (3).
1. Burgering BM and Kops GJ Trends Biochem Sci. 27(7):352-360, 2002.
2. Huang H and Tindall DJ Future Oncol 2(1):83-89, 2006.
3. Riou C et al. JEM 204(1):79-91, 2006.
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