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 so much attention-grabbing period of recent melanoma learn and molecular biology, an period that continues to be in complete swing and doesn't express any symptoms of finishing within the foreseeable destiny. p53 has emerged as a key tumor suppressor and significant objective for novel melanoma treatment. For round 10 years, p53 was once thought of an oncogene with a bit strange positive factors. despite the fact that, a massive paradigm shift happened round 1988-89 whilst interesting new findings verified that standard (wild variety) 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. actually, p53 seemed to be the main usually mutated gene in melanoma cells. next paintings in the course of 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 telephone. This ebook, written by way of world-leading p53 researchers together with a lot of those that have formed the sphere over the last 25 years, offers particular insights into the growth of the p53 box and the clients for higher melanoma analysis and remedy sooner or later. it may be of curiosity to every person operating in melanoma examine, scientific oncology, and molecular biology, and certainly to anyone drawn to technological know-how, drugs, in addition to in contemporary advancements of the guidelines and ideas of the molecular biology of melanoma.

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On a related note, Flores et al. , 2002). They were able to show that removal of the p63 and p73 genes resulted in a decreased occupancy of p53 at apoptotic promoters, although the precise function/mechanism of the p53 homologs in this context is still elusive. , 2001). The idea that the sequence-specific binding function of p53 is the only activity targeted in oncogenesis could be somewhat over-simplified. , 2003), two anti-apoptotic proteins that reside in the outer mitochondrial membrane and protect its integrity (reviewed in Green & Evan, 2002).

P53 is also capable of transrepression of some genes although the mechanisms are less well-understood (reviewed in Oren, 2003). , 2003), other mechanisms involving direct repression have also been described. , 2001). However some cis-acting DNA sequences required for p53-transrepression have also been identified. Some of these sequences conform to the consensus p53 binding site while others are essentially permutations of the consensus. The first class of repression target sequences found in the Bcl-2 and α-fetoprotein genes contains p53 binding 2.

Cancer risks from germline p53 mutations. Journal of Clinical Investigation, 1992. 90: 1637-1641. P, A human DNA segment with properties of the gene that predisposes to retinoblastoma and osteosarcoma. Nature, 1986. 323: 643-646. W. A transcriptionally active DNAbinding site for human p53 protein complexes. Molecular and Cellular Biology, 1992. 12: 2866-2871. K. Ataxia-telangiectasia-mutated (ATM) and NBS1-dependent phosphorylation of Chk1 on Ser-317 in response to ionizing radiation. Journal of Biological Chemistry, 2003.

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


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