a transcriptional activator factor. Contains 1 fork-head domain. May play a role in the control of cell proliferation. Appears to be expressed only in adult organs containing proliferating/cycling cells or in response to growth factors. Also expressed in epithelial cell lines derived from tumors. Not expressed in resting cells. Phosphorylated in M (mitotic) phase. Three splice variant isoforms have been described. Isoform 1 and isoform 2 appear to be the only activators of gene transcription. Isoform 3, found in rat, does not seem to exist in human. Note: This description may include information from UniProtKB.
Protein type: DNA binding protein; Transcription factor
Molecular Function: RNA polymerase II transcription factor activity, enhancer binding; protein binding; DNA binding; sequence-specific DNA binding; double-stranded DNA binding; transcription factor binding; protein kinase binding; transcription factor activity; DNA bending activity
Biological Process: regulation of Ras protein signal transduction; transcription from RNA polymerase II promoter; tissue development; regulation of cell cycle; positive regulation of transcription, DNA-dependent; negative regulation of transcription from RNA polymerase II promoter; liver development; DNA repair; negative regulation of stress-activated MAPK cascade; cell cycle; pattern specification process; regulation of cell proliferation; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; embryonic development; regulation of transcription factor activity; regulation of transcription, DNA-dependent; positive regulation of cell proliferation; positive regulation of transcription from RNA polymerase II promoter; regulation of cell growth; mitotic cell cycle; negative regulation of transcription, DNA-dependent; vasculogenesis; G2/M transition of mitotic cell cycle
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.