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Abstract

Tumor suppressor protein p53 plays a central role in maintaining genomic integrity. p53 induces cell cycle arrest and apoptosis by transactivating the expression of downstream target genes in response to genotoxic stress. Tetramer formation of p53 is essential for its activity. The aims of this study were to reveal the dysfunction threshold of p53 caused by destabilization of its tetrameric structure. In Chap. 2, we demonstrated that a relatively small destabilization of the tetrameric structure by the missense mutation could induce significantly decreased amounts of the tetramer in the nucleus. In Chaps. 3 and 4, functional control of p53 via tetramer formation was performed; in Chap. 3, tumor-associated mutants were rescued by stabilization of the tetrameric structure using calixarene derivatives and in Chap. 4, transcriptional activity of p53 was inhibited by hetero-oligomerization.

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Correspondence to Rui Kamada .

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Kamada, R. (2012). General Introduction. In: Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53. Springer Theses. Springer, Tokyo. https://doi.org/10.1007/978-4-431-54135-6_1

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