25 Years of P53 Research by Pierre Hainaut, Klas G. Wiman

By Pierre Hainaut, Klas G. Wiman

The invention of p53 in 1979 marks the start of a so much attention-grabbing period of recent melanoma study and molecular biology, an period that remains in complete swing and doesn't exhibit any symptoms of finishing within the foreseeable destiny. p53 has emerged as a key tumor suppressor and critical objective for novel melanoma treatment. For round 10 years, p53 was once thought of an oncogene with just a little strange positive aspects. although, a massive paradigm shift happened round 1988-89 while intriguing new findings verified that ordinary (wild style) p53 may perhaps inhibit transformation of cells in tradition and that the p53 gene used to be mutated in a wide fraction of human tumors. in truth, p53 looked to be the main often mutated gene in melanoma cells. next paintings through the 1990’s confirmed that p53 was once a transcription issue that regulates many different genes, and that p53 can set off apoptosis, the suicide application of the mobilephone. This e-book, written through world-leading p53 researchers together with a lot of those that have formed the sphere over the last 25 years, presents specific insights into the growth of the p53 box and the customers for higher melanoma analysis and treatment sooner or later. it's going to be of curiosity to every body operating in melanoma study, scientific oncology, and molecular biology, and certainly to anyone attracted to technology, drugs, in addition to in contemporary advancements of the information and ideas of the molecular biology of melanoma.

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The N terminus of p53 regulates its dissociation from DNA. J Biol Chem 2000; 275:39944-53. , Scolnick D. , Ying C. , Halazonetis T. , Berger S. L. Two tandem and independent sub-activation domains in the amino terminus of p53 require the adaptor complex for activity. Oncogene 1997; 15:807-16. , Ng H. , Sekinger E.

Proceedings of the National Academy of Sciences USA, 2002. 99: 8467-8472. C. p53 mutations in human cancers. Science, 1991. 253: 49-53. , Yasuda H. Oncoprotein MDM2 is a ubiquitin ligase E3 for tumor suppressor p53. , 1997. 420: 25-27. , Distinct p53-mediated G1/S checkpoint responses in two NIH3T3 subclone cells following treatment with DNAdamaging agents. Oncogene, 1996. 13: 625-632. A. Tumor spectrum analysis in p53- deficient mice. Current Biology, 1994. 4: 1-7. G. Transcriptional response off lymphoblastoid cells to ionizing radiation.

Printed in the Netherlands. 28 Chapter 2 R248 R273 R175 G245 R249 AD1 1 20 AD2 40 R282 PXXP 60 TETRA 90 97 100 300 320 360 363 393 Figure 1. fr/p53). Indicated are the N-terminal activation domains (AD1, AD2), the proline rich region (PXXP), the central core sequence specific DNA binding domain (DNA BINDING CORE), the tetramerization domain (TETRA) and the C-terminal sequence non-specific nucleic acid binding region (BASIC). TRANSACTIVATION DOMAIN The first 100 amino acids of p53 contain two transactivation domains, a proline-rich domain and a nuclear export signal.

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