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 have been identified in MCF-7, a breast carcinoma cell line. These mRNAs code for variant p73 proteins bearing distinct C-terminal structures suggesting that the C-terminal region of p73 may be important for its function. A p73 variant has been identified that lacks an N-terminal transactivation domain, called δNp73. The δNp73 message is transcribed from an alternative promoter located in intron 3.
Levrero M. et al. (2000) J Cell Sci. 113 (10):1661.
Ueda Y. et al. (1999) Oncogene. 18:4993.
Kaghad M. et al. (1997) Cell. 90:809.
*For more information, see UniProt Accession O15350
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*All molecular weights (MW) are confirmed by comparison to Bio-Rad Rainbow Markers and to western blot mobilities of known proteins with similar MW.
This kit contains: