Anti-FOXO3A

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Forkhead box O3, also known as FKHRL1 or FOXO3A, is a human protein encoded by the FOXO3 gene. FOXO3A belongs to the O subclass of the forkhead family of transcription factors which are characterized by a distinct fork head DNA-binding domain. It is mapped to 6q21. This protein likely functions as a trigger for apoptosis through upregulation of genes necessary for cell death, such as Bim andPUMA, or downregulation of anti-apoptotic proteins such as FLIP. In mammals FOXO3A regulates the resistance of cells to stress by inducing DNA repair and thereby may also affect organismal life span. In addition, it is thought that FOXO3A is also involved in protection from oxidative stress by upregulating antioxidants such as catalase and MnSOD. Protein function: Transcriptional activator that recognizes and binds to the DNA sequence 5'-[AG]TAAA[TC]A-3' and regulates different processes, such as apoptosis and autophagy (PubMed:10102273, PubMed:16751106, PubMed:21329882, PubMed:30513302). Acts as a positive regulator of autophagy in skeletal muscle: in starved cells, enters the nucleus following dephosphorylation and binds the promoters of autophagy genes, such as GABARAP1L, MAP1LC3B and ATG12, thereby activating their expression, resulting in proteolysis of skeletal muscle proteins. Triggers apoptosis in the absence of survival factors, including neuronal cell death upon oxidative stress (PubMed:10102273, PubMed:16751106). 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). In response to metabolic stress, translocates into the mitochondria where it promotes mtDNA transcription. 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. Also acts as a key regulator of regulatory T-cells (Treg) differentiation by activating expression of FOXP3 (PubMed:30513302). [The UniProt Consortium]