Transcriptional activator which probably serves as a general switch factor for erythroid development. It binds to DNA sites with the consensus sequence [AT]GATA[AG] within regulatory regions of globin genes and of other genes expressed in erythroid cells. May form homodimers or heterodimers with other isoforms. Interacts (via the N-terminal zinc finger) with ZFPM1. Interacts with GFI1B. Interacts with PIAS4; the interaction enhances sumoylation and represses the transactivational activity in a sumoylation-independent manner. Interacts with LMCD1. Interacts with CREBBP; the interaction stimulates acetylation and transcriptional activity in vivo. Interacts with EP300. Erythrocytes. 3 isoforms of the human protein are produced by alternative splicing. Note: This description may include information from UniProtKB.
Molecular Function: chromatin DNA binding; DNA bending activity; DNA binding; p53 binding; protein binding; sequence-specific DNA binding; transcription factor activity; zinc ion binding
Biological Process: basophil differentiation; blood coagulation; cell-cell signaling; embryonic hemopoiesis; eosinophil differentiation; erythrocyte development; erythrocyte differentiation; gut development; heart development; homeostasis of number of cells within a tissue; in utero embryonic development; male gonad development; megakaryocyte differentiation; negative regulation of apoptosis; negative regulation of bone mineralization; negative regulation of cell proliferation; negative regulation of transcription from RNA polymerase II promoter; organ morphogenesis; platelet formation; positive regulation of erythrocyte differentiation; positive regulation of osteoblast proliferation; positive regulation of peptidyl-tyrosine phosphorylation; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; tissue development; transcription from RNA polymerase II promoter
LTP: 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.