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Overexpression of HAUSP results in p53 stabilization. However, depletion of HAUSP does not result in a decrease in p53 levels but rather increases p53 levels due to the fact that HAUSP binds and deubiquitinates Mdm2. It has been shown that HAUSP is a better binding partner to Mdm2 than p53 in unstressed cells.
Many cancers exhibit mutations in the p53 gene, but this mutation can only be detected through extensive DNA sequencing. Studies have shown that cells with p53 mutations have significantly lower levels of PUMA, making it a good candidate for a protein marker of p53 mutations, providing a simpler method for testing for p53 mutations. [44]
P53, p63, and p73 have similar features in their gene structures and functions but have also diverged evolutionarily. The p53 family evolved from an ancestor gene in unicellular life. [ 4 ] The ancestor gene functioned in germ line DNA protection early invertebrates. [ 5 ]
However, under high levels of cellular stress TIGAR expression decreases. [12] P53, a transcription factor, can bind two sites within the human TIGAR gene to activate expression. [9] [13] One site is found within the first intron, and binds p53 with high affinity.
Mdm2 also acts as an E3 ubiquitin ligase, targeting both itself and p53 for degradation by the proteasome (see also ubiquitin). Several lysine residues in p53 C-terminus have been identified as the sites of ubiquitination, and it has been shown that p53 protein levels are downregulated by Mdm2 in a proteasome-dependent manner. Mdm2 is capable ...
Apoptosis-stimulating of p53 protein 2 (ASPP2) also known as Bcl2-binding protein (Bbp) and tumor suppressor p53-binding protein 2 (p53BP2) is a protein that in humans is encoded by the TP53BP2 gene. [ 5 ] [ 6 ] [ 7 ] Multiple transcript variants encoding different isoforms have been found for this gene.
Lahav developed a novel system for following p53 levels and Mdm2 levels simultaneously in individual living cells [2] and demonstrated that individual cells show discrete pulses of p53 after gamma irradiation. Genetically identical cells showed different numbers of pulses: 0, 1, 2 or more.
It was shown that, although p53 arrests the numbers of cells to different extents in different phases, the measured level of survivin mRNA and protein levels were the same across all the samples transfected with the wild-type p53. This shows that p53 acts in a cell-cycle independent manner to inhibit survivin expression. [17]