Transcription factor that regulates metabolic homeostasis in response to oxidative stress. Binds to the 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'. Main regulator of redox balance and osteoblast numbers and controls bone mass. Orchestrates the endocrine function of the skeleton in regulating glucose metabolism. 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. 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. Shuttles between the cytoplasm and nucleus. Localized to the animal hemisphere during early cleavage stages. At early tadpole stages, expressed in the branchial arches, pronephros and liver. Within the head, expressed in the forming thyroid gland and in head mesenchyme anterior to the eyes. Expressed both maternally and zygotically. Maternal expression decreases during early cleavage stages becoming absent during gastrulation. Zygotic expression begins during neurulation with expression levels increasing as development progresses. Phosphorylated by AKT1; insulin-induced. IGF1 rapidly induces phosphorylation of Thr-28, Ser-245 and Ser-308. Phosphorylation of Ser-245 decreases DNA-binding activity and promotes the phosphorylation of Thr-28, and Ser-308, which leads to nuclear exclusion and loss of function. Phosphorylation of Ser-318 is independent of IGF1 and leads to reduced function (By similarity).