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The p53 tumor suppressor protein activates transcription and induces cell death. A close homologue of p53, termed p73, is expressed in transactivating (TA) forms that induce growth arrest and apoptosis much like p53. However, the p73 gene contains a second promoter, giving rise to the expression of p73 Delta N, a species of p73 proteins that lack the(More)
The gene PIG3 is induced by the tumor suppressor p53 but not by p53 mutants unable to induce apoptosis, suggesting its involvement in p53-mediated cell death. Here we show that p53 directly binds and activates the PIG3 promoter, but not through the previously described DNA element. Instead, p53 interacts with a pentanucleotide microsatellite sequence within(More)
The transcriptionally active forms of p73 are capable of inducing apoptosis, and the isoforms termed TAp73 are important players when E2F and its oncogenic activators induce programmed cell death. However, the conditions under that TAp73 can kill a cell remain to be clarified. Recently, it has been found that p73 proteins are not merely floating in the(More)
The most frequent genetic alteration in cancer is a mutation of p53. In most cases, this leads to a sharp increase of the p53 protein levels but abolishes p53's function as an activator of transcription. To correct this defect, wild-type p53 is being reintroduced into tumor cells through gene therapy vectors, thereby inducing cell death. However, this(More)
The E1B-55 kDa oncoprotein of adenovirus type 5 targets the tumor suppressor protein p53. This includes four distinct activities: (i) biochemical interaction of E1B-55 kDa with p53; (ii) inhibition of p53-induced transcription; (iii) relocalization of p53 from the nucleus to the cytoplasm; and (iv) in the simultaneous presence of E1B-55 kDa and the(More)
The feature-interaction problem has been explored for many years. Still, we lack sufficient knowledge about the interplay of different kinds of interactions in software product lines. Exploring the relations between different kinds of feature interactions will allow us to learn more about the nature of interactions and their causes. This knowledge can then(More)
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