a member of the E2F/DP family of transcription factors.The E2F family plays a crucial role in the control of cell cycle and action of tumor suppressor proteins and is also a target of the transforming proteins of small DNA tumor viruses. Binds DNA cooperatively with Dp transcription factors in the promoter region of a number of genes whose products are involved in cell cycle regulation or in DNA replication.The Dp-1/E2F complex functions in the control of cell-cycle progression from G1 to S phase. The E2F-1 complex binds specifically hypophosphorylated retinoblastoma protein RB1. During the cell cycle, RB1 becomes phosphorylated in mid-to-late G1 phase, detaches from the DRTF1/E2F complex, rendering E2F transcriptionally active. Phosphorylated by CDK2 and cyclin A-CDK2 in the S-phase. It can mediate both cell proliferation and p53-dependent apoptosis. Note: This description may include information from UniProtKB.
Protein type: DNA binding protein; Transcription factor
Molecular Function: protein binding; DNA binding; sequence-specific DNA binding; transcription factor activity; transcription corepressor activity; transcription factor binding
Biological Process: Notch signaling pathway; transcription, DNA-dependent; apoptosis; positive regulation of transcription, DNA-dependent; mRNA stabilization; negative regulation of transcription from RNA polymerase II promoter; G2 phase of mitotic cell cycle; anoikis; cell proliferation; positive regulation of fibroblast proliferation; DNA damage response, signal transduction resulting in induction of apoptosis; regulation of transcription, DNA-dependent; forebrain development; DNA damage checkpoint; spermatogenesis; positive regulation of transcription from RNA polymerase II promoter; mitotic cell cycle; negative regulation of transcription, DNA-dependent; G1 phase of mitotic cell cycle; G1/S 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.