p73 was identified as a long-lost cousin of tumor suppressor protein, p53. p73 has high homology with p53 as well as with p63, a gene implicated in the maintenance of epithelial stem cells. Significant homology between p53, p63, and p73 (approximately 63% amino acid identity in the DNA-binding domain suggest that they may have overlapping functions in the regulation of gene expression. The targeted disruption of p73 gene leads to defects hippocampal dysgenesis, hydrocephalus, chronic inflammation and infections. Recently, spilicing variant mRNAs of p73 has been identified in MCF-7, a breast carcinoma cell line. These mRNAs code for variant p73 proteins bearing distinct carboxy-terminal structures suggesting that the carboxy-terminal region of p73 may be important for the functions of this protein. Recently, Yang et al. (2000) have cloned a p73 variant that lacks an amino-terminal transactivation domain, called deltaNp73. The dNp73 message is transcribed from an alternative promoter located in intron 3.
							
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