P53 Protocols
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p53 Protocols
Author: Sumitra Deb
language: en
Publisher: Springer Science & Business Media
Release Date: 2008-02-02
Since the discovery of p53 as a tumor suppressor, numerous methods have evolved to reveal the unique structural features and biochemical functions of this protein. Several unique properties of p53 posed a challenge to understa- ing its normal function in the initial phase of its research. The low levels of p53 in normal cells, its stabilization under situations of genotoxic stress, induction of growth arrest, and apoptosis with stabilization of the protein, obstructed the visibility of its normal, unmutated function. The property of p53 that can sense a promoter and transactivate or inhibit is still not well understood. It is still not known whether it is the absence of the protein that causes tumorigenesis, or if its mutants have a dominant role in inducing cancer. p53 Protocols comprises eighteen chapters for the study of the diverse properties of p53 and related proteins. The methods included are invaluable for delineating the function of other proteins that may function as tumor suppr- sors or growth suppressors. The chapters are not presented in any schematic order, for the importance and diversity of the functions of p53 make it imp- sible to organize them suitably. We have made a sincere effort to collect the methods most useful to those investigators working on tumor suppressors or growth suppressors. The purpose of p53 Protocols is not only to provide investigators with methods to analyze similar biochemical functions, but also to familiarize them with the associated problems that arose during the course of investigations.
SV40 Protocols
Author: Leda Raptis
language: en
Publisher: Springer Science & Business Media
Release Date: 2008-02-02
Simian virus 40 gained notoriety in the 1960s because it was found to be a contaminant of polio and adenovirus vaccines that had been administered to millions of healthy individuals worldwide. The public health implications of this revelation provided the initial impetus for an in-depth study of SV40 biology. Later work showed that SV40 DNA sequences as well as infectious virus are in fact found in human tumors and may have contributed to oncog- esis. It also turned out that SV40 uses mostly cellular machinery to carry out many steps in viral infection, which makes it a powerful probe for examining many fundamental questions in eukaryotic molecular biology. SV40 Pro- cols consolidates a number of well-tested step-by-step techniques in one v- ume; experts with hands-on experience in particular methods give detailed accounts of their optimized experimental protocols, so that the beginner, as well as more experienced researchers, may readily overcome problems of ambiguity often present in the literature. As with other DNA tumor viruses, the response of cultured cells to SV40 infection depends upon the species being infected. Monkey cells s- port virus production, which leads to their death, whereas rodent cells p- duce only the early proteins and acquire a transformed phenotype. Thus, SV40 Protocols is organized in two sections. The first relates to assays of the lytic cycle of the virus, and the second deals with transformation.
Molecular Toxicology Protocols
Author: Phouthone Keohavong
language: en
Publisher: Springer Science & Business Media
Release Date: 2008-02-03
A collection of cutting-edge techniques for analyzing genotoxic exposure and detecting the resulting biological effects-including endogenous metabolites-up to and including the development of cancer. The authors emphasize analytical methods that can be specifically applied to human populations and patients. Among the applications detailed are the analysis of interactions between such cellular macromolecules as DNA and proteins and chemical and physical agents, the assessment of medically relevant toxicity, and the characterization of genetic alterations induced in transgenic animals by in vivo systems. There are also methods for the analysis of genotoxic exposure during gene expression, of cytotoxicity caused by the induction of apoptosis, of genetic alterations in reporter genes and oncogenes, early (premalignant) detection of altered oncogenes, and of individual variation in biotransformation and DNA repair capacity.