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Tetramer Stability and Functional Regulation of Tumor Suppressor Protein p53

Part of the Springer Theses Book Series

DOI: 10.1007/978-4-431-54135-6

ISBN: 978-4-431-54134-9

Publisher: Springer Japan - Springer Journals

Jul 21, 2012

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Chapter 1General Introduction

Kamada, Rui

Pages: 1 –12

[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...
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Chapter 2Quantitative Analysis for p53 Tetramerization Domain Mutants Reveals a Low Threshold for Tumor Suppressor Inactivation

Kamada, Rui

Pages: 13 –43

[The tumor suppressor p53, a 393 amino acid transcription factor, induces cell cycle arrest and apoptosis in response to genotoxic stress. Its inactivation via the mutation of its gene is a key step in tumor progression, and tetramer formation is critical for p53 post-translational modification...
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Chapter 3Stabilization of Mutant Tetrameric Structures by Calixarene Derivatives

Kamada, Rui

Pages: 45 –59

[Li-Fraumeni syndrome, a hereditary disorder characterized by familial clusters of early-onset multiple tumors, is caused by mutation of the TP53 gene, which encodes the p53 tumor suppressor protein. Mutation of Arg337 to histidine in the tetramerization domain of p53 is most frequently observed...
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Chapter 4Inhibition of the Transcriptional Activity of p53 Through Hetero-Oligomerization

Kamada, Rui

Pages: 61 –70

[Induced pluripotent stem (iPS) cells can be generated by the expression of pluripotency factors and oncogenes; however, the efficiency of generating iPS cells is extremely low (less than 1 %). Activation of the p53-p21 pathway is responsible for this low efficiency and inactivation of p53...
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Chapter 5Conclusion

Kamada, Rui

Pages: 71 –72

[p53 tetramer formation is essential for DNA binding, post-translational modification, and protein–protein interaction. To clarify the threshold for dysfunction of p53 in terms of the destabilization of p53’s tetrameric structure, this study focused on the effects of tumor-associated mutations in...

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