a protein of the p53 family of proteins. p73, like p53, may have tumor suppressor activity, but its multiple isoforms possess different and sometimes opposing functions. Participates in the apoptotic response to DNA damage. Phosphorylated in a cell cycle-dependent manner and negatively regulated by CDKs. When overproduced, activates transcription from p53-responsive promoters and induces apoptosis. Nine transactivation competent (TA) or dominant negative (DN) isoforms, derived from alternative-splicing and alternative promoters, have been described. NH2-terminally truncated p73 isoforms (DNp73) may be oncogenic. DNp73 is elevated in a number of cancers and is associated with adverse clinical outcomes and resistance to chemotherapy. The C-terminal oligomerization domain binds to the ABL1 tyrosine kinase SH3 domain. Isoform Beta interacts homotypically and with p53/TP53, whereas isoform Alpha does not. Isoform Gamma interacts homotypically and with all p73 isoforms. Isoform Delta interacts with isoform Gamma, isoform Alpha, and homotypically. Isoforms Alpha and Beta interact with HIPK2. Isoform Alpha interacts with RANBP9; forms complex with p53 and CABLES1. Isoform Beta interacts with WWOX; interacts with HECW2. Note: This description may include information from UniProtKB.
Protein type: DNA-binding; Tumor suppressor; Transcription factor
Molecular Function: chromatin binding; damaged DNA binding; identical protein binding; p53 binding; protein binding; protein kinase binding; transcription factor activity; transcription factor binding
Biological Process: DNA damage response, signal transduction by p53 class mediator resulting in induction of apoptosis; DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator; DNA damage response, signal transduction resulting in induction of apoptosis; G1 DNA damage checkpoint; mismatch repair; negative regulation of cardiac muscle cell proliferation; negative regulation of JNK activity; negative regulation of neuron apoptosis; negative regulation of transcription from RNA polymerase II promoter; positive regulation of transcription from RNA polymerase II promoter; positive regulation of transcription, DNA-dependent; regulation of apoptosis; regulation of gene expression; regulation of mitotic cell cycle; response to DNA damage stimulus; response to gamma radiation; response to X-ray
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.