TP73

This gene encodes a member of the p53 family of transcription factors involved in cellular responses to stress and development. It maps to a region on chromosome 1p36 that is frequently deleted in neuroblastoma and other tumors, and thought to contain multiple tumor suppressor genes. The demonstration that this gene is monoallelically expressed (likely from the maternal allele), supports the notion that it is a candidate gene for neuroblastoma. Many transcript variants resulting from alternative splicing and/or use of alternate promoters have been found for this gene, but the biological validity and the full-length nature of some variants have not been determined. [provided by RefSeq, Feb 2011]

TP73

Participates in the apoptotic response to DNA damage. Isoforms containing the transactivation domain are pro-apoptotic, isoforms lacking the domain are anti-apoptotic and block the function of p53 and transactivating p73 isoforms. May be a tumor suppressor protein. Is an activator of FOXJ1 expression (By similarity).
It is an essential factor for the positive regulation of lung ciliated cell differentiation (PubMed:34077761).

Biological Process cell cycle Source:UniProtKB-KW
Biological Process cellular response to DNA damage stimulus Source:UniProtKB1 Publication
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage Source:ProtInc1 Publication
Biological Process intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source:UniProtKB2 Publications
Biological Process kidney development Source:Ensembl
Biological Process mismatch repair Source:ProtInc1 Publication
Biological Process negative regulation of cardiac muscle cell proliferation Source:MGI1 Publication
Biological Process negative regulation of cell population proliferation Source:AgBase
Biological Process negative regulation of neuron differentiation Source:Ensembl
Biological Process positive regulation of apoptotic process Source:Ensembl
Biological Process positive regulation of DNA-templated transcription Source:UniProtKB1 Publication
Biological Process positive regulation of lung ciliated cell differentiation Source:UniProtKB1 Publication
Biological Process positive regulation of MAPK cascade Source:Ensembl
Biological Process positive regulation of oligodendrocyte differentiation Source:Ensembl
Biological Process positive regulation of transcription by RNA polymerase II Source:UniProtKB3 Publications
Biological Process protein tetramerization Source:InterPro
Biological Process regulation of cell cycle Source:ParkinsonsUK-UCL1 Publication
Biological Process regulation of gene expression Source:MGI1 Publication
Biological Process regulation of mitotic cell cycle Source:MGI1 Publication
Biological Process regulation of transcription by RNA polymerase II Source:GO_Central1 Publication
Biological Process response to organonitrogen compound Source:Ensembl
Biological Process response to xenobiotic stimulus Source:Ensembl

Nucleus
Cytoplasm
Accumulates in the nucleus in response to DNA damage.

Ciliary dyskinesia, primary, 47, and lissencephaly (CILD47):
A form of primary ciliary dyskinesia, a disorder characterized by abnormalities of motile cilia. Respiratory infections leading to chronic inflammation and bronchiectasis are recurrent, due to defects in the respiratory cilia. CILD47 is an autosomal recessive form characterized by onset soon after birth or in early childhood. Affected individuals also have neurologic features, such as impaired intellectual development and central hypotonia, associated with structural brain abnormalities, most notably lissencephaly and thin or absent corpus callosum. No situs abnormalities have been observed.

Isoform alpha (but not isoform beta) is sumoylated on Lys-627, which potentiates proteasomal degradation but does not affect transcriptional activity. Phosphorylation by PLK1 and PLK3 inhibits the transcription regulator activity and pro-apoptotic function.
Higher levels of phosphorylation seen in the brain from patients with Huntington disease.
Polyubiquitinated by RCHY1/PIRH2; leading to its degradation by the proteasome.