Read e-book online 25 Years of P53 Research PDF

By Pierre Hainaut, Klas G. Wiman

ISBN-10: 1402029209

ISBN-13: 9781402029202

ISBN-10: 1402029225

ISBN-13: 9781402029226

The invention of p53 in 1979 marks the start of a such a lot interesting period of contemporary melanoma study and molecular biology, an period that remains in complete swing and doesn't convey any symptoms of finishing within the foreseeable destiny. p53 has emerged as a key tumor suppressor and significant aim for novel melanoma remedy. For round 10 years, p53 was once thought of an oncogene with just a little strange gains. even though, an immense paradigm shift happened round 1988-89 whilst fascinating new findings validated that ordinary (wild kind) p53 may well 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 software of the mobile. This booklet, written through world-leading p53 researchers together with lots of those that have formed the sector during the last 25 years, offers precise insights into the growth of the p53 box and the clients for greater melanoma prognosis and treatment sooner or later. it's going to be of curiosity to all people operating in melanoma learn, scientific oncology, and molecular biology, and certainly to anyone drawn to technology, medication, in addition to in contemporary advancements of the information and ideas of the molecular biology of melanoma.

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Extra info for 25 Years of P53 Research

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This domain is responsible for the mostly tetrameric state of p53 in solution and along with the basic region comprises the minimal transforming domain. The structure of the tetramerization domain has been determined and forms a “dimer of dimers” which folds/assembles in the same manner. e. each dimer binds two contiguous quarter-sites of the target sequence. , 1999). , 1990). Interestingly, the tetrameric status of p53 requires a larger hydrophobic side chain at residue 341 than 344. An inversion of this relationship results in dimeric p53.

Cell, 1989. 56: 67-75. J. The p53-mdm-2 autoregulatory feedback loop. Genes and Development, 1993. 7: 1126-1132. , Beach D. p21 is a universal inhibitor of cyclin kinases. Nature, 1993. 366: 701-704. , Experimental study off the pathogenesis of carcinoma. Journal of Cancer Research, 1918. 3: 1-29. , Rannala B, Likelihood models of somatic mutation and codon substitution in cancer genes. Genetics, 2003. 165: 695-705. , Oren M. Sequence-specific DNA binding by p53: identification of target sites and lack k of binding to p53-MDM2 complexes.

Biol. , 1984. 2: 261-272. M. SV40 large tumor antigen forma a specific complex with the product of the retinoblastoma susceptibility gene. Cell, 1988. 54: 275-283. J, Detection of a transformation-related antigen in chemically-induced sarcomas and other transformed cells of the mouse. Proceedings of the National Academy of Sciences USA, 1979. 76: 24202424. DeOme K. Formal discussion of: multiple factors in mouse mammary tumorigenesis. Cancer Research, 1965. 25: 1348-1351. J. p53 gain of function mutations.

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

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