By Pierre Hainaut, Klas G. Wiman
P53 has emerged as a key tumor suppressor and significant goal for novel melanoma remedy. This e-book, written through world-leading p53 researchers together with lots of those that have formed the sector during the last 25 years, presents detailed insights into the development of the sector and the clients for larger melanoma prognosis and remedy sooner or later.
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Extra resources for 25 Years of P53 Research
134: 477-482. P. owth control by p53? Bioessays, 1993. 15:. 689-690. K. Increased sequence-specific p53-DNA binding activity after DNA damage is attenuated by phorbol esters. Oncogene, 1993. 8:. 3055-3062. , Lozano G. Transcriptional activation by wild-type but not transforming mutants of the p53 anti-oncogene. Science, 1990. 249: 1049-1051. , Sun Y. Global genechip profiling to identify genes responsive to p53-induced growth arrest and apoptosis in human lung carcinoma cells. Cancer Biol. , 2003.
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Regulation of p53 DNA Binding 37 BASIC DOMAIN An extraordinary amount of research has focused on the last 30 amino acids of p53. , 1991; Wang Y. , 1993). , 1999) and many other stress-inducible modification sites including phosphorylation, acetylation and glycosylation (reviewed in Appella & Anderson, 2001). The extreme C-terminus of p53 has long been a focus of experiments addressing the regulation of sequence-specific DNA binding (reviewed in Ahn & Prives, 2001). , 1994; Jayaraman & Prives, 1995), insertion/deletion mismatches (Lee S.
25 Years of P53 Research by Pierre Hainaut, Klas G. Wiman