The p73 exhibits sequence homology to the p53's transcriptional activation, DNA binding, and oligomerization domains. However, adenovirus E1B 55K, simian virus 40 T, and human papillomavirus E6 do not physically interact with p73 indicating that the functions of these two proteins may differ under physiological conditions. 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. p73 is expressed in either a full length form (a) (MW ~80kD) or a shorter (b) (MW ~70kD) mRNA variant, with exon 13 spliced out. Transient overexpression of p73 in cells can induce apoptosis and p21, a cellular p53 target gene primarily responsible for p53 dependent cell cycle arrest. The targeted disruption of p73 gene leads to defects hippocampal dysgenesis, hydrocephalus, chronic inflammation and infections. p73 is upregulated in a significant fraction of anaplastic thyroid cancers, whereas it is not detectable in normal thyroid epithelial cells nor in papillary or follicular thyroid cancer.
Recombinant Human p73 beta protein images
SDS-PAGE - p73 beta protein (ab102553)
SDS-PAGE showing ab102553 at approximately 88kDa.
References for Recombinant Human p73 beta protein (ab102553)
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