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Bacterial Protein Toxins
Bacterial toxins that act inside cells interact very specifically with key components of the cell and some even manipulate the cell in subtle ways for their own purposes. These potent toxins, described in this 2005 book, will be of interest to both microbiologists and cell biologists. Some of these toxins are conventional multidomain toxins that are self-programmed to enter cells. Others are delivered by type III mechanisms, often as a package of potent molecules. The molecular targets for all these toxins mediate signal transduction and the cell cycle to regulate the crucial processes of cell growth, cell division and differentiation. Thus these potent toxins are not only responsible for disease, but also provide a powerful set of tools with which to interrogate the biology of the cell. In addition such toxins may act directly to promote carcinogenesis and hence their study is also of interest in a wider context.
Encyclopedia of Molecular Pharmacology
An essential text, this is a fully updated second edition of a classic, now in two volumes. It provides rapid access to information on molecular pharmacology for research scientists, clinicians and advanced students. With the A-Z format of over 2,000 entries, around 350 authors provide a complete reference to the area of molecular pharmacology. The book combines the knowledge of classic pharmacology with the more recent approach of the precise analysis of the molecular mechanisms by which drugs exert their effects. Short keyword entries define common acronyms, terms and phrases. In addition, detailed essays provide in-depth information on drugs, cellular processes, molecular targets, techniques, molecular mechanisms, and general principles.
GTPases
GTPases are molecular switches that are used to control biochemical pathways. This book describes the properties and cellular roles of all the major families of GTPases. All cells use GTPases to regulate the delivery of amino acids to the ribosome during protein synthesis, but eukaryotes, with their complex and compartmentalized environment, have exploited the versatility of GTPases to a much greater extent. In particular, GTPases play a central role in regulating signal transduction pathways activated by extracellular signals and in regulating the trafficking of proteins beetween different organelles. It is not surprising, therefore, that GTPases have become a center of attention for those studying the control of proliferation, differentiation, cell polarity, cell movement, and vesicle and protein trafficking. This book provides a complete guide to this area and should be essential reading for cell and molecular biologists, biochemists and geneticists interested in these contemporary problems.
Ras Superfamily Small G Proteins: Biology and Mechanisms 1
This first of two volumes provides a general overview of the genetics, structure, mechanism and regulation of the Ras superfamily proteins and describes in detail the signaling pathways and processes regulated by specific members of this family. The focus of this first volume is on the Rho and Ras subfamily of small G proteins. Renowned scientists provide insights into the biochemistry of the classical and non-classical small G-protein family members, their spatio-temporal regulation, their effectors and their roles in health and disease. Together with Volume 2, this book provides a comprehensive and state-of-the-art work on small G-proteins (GTPases). It is intended for graduates and professors in biochemistry and cell biology already working on small G-proteins (small GTPases), but also offers an extremely valuable resource for those readers who are new to the field.
Special Issue on Emerging Bacterial Toxins
With contributions by numerous experts
RhoA/C Inhibits Proliferation by Inducing the Synthesis of GPRC5A
Abstract: Rho GTPases are important regulators of many cellular functions like cell migration, adhesion and polarity. The molecular switches are often dysregulated in cancer. We detected Rho-dependent upregulation of the orphan seven-transmembrane receptor G-protein-coupled receptor family C group 5 member A (GPRC5A). GPRC5A is highly expressed in breast cancer whereas in lung cancer, it is often downregulated. Here, we analyzed the function of GPRC5A in breast epithelial and breast cancer cells. Activation or expression of RhoA/C led to GPRC5A-dependent inhibition of proliferation and reduction of the colony forming capacity of benign breast epithelial cells. This effect is based on an inhibition of EGFR signalling. Knockout of retinoic acid induced 3 (RAI3, the gene for GPRC5A) in breast cancer cells increased cell division, whereas Rho activation had no effect on proliferation. Knockout of RAI3 in benign breast epithelial cells led to decrease of EGFR expression and diminished proliferation
Regulators and Effectors of Small GTPases, Part D: Rho Family
This volume and its companions (Volumes 255, 256, 257, and the forthcoming 329) cover all biochemical and biological assays currently in use for analyzing the role of small GTPases in these aspects of cell biology at the molecular level.The critically acclaimed laboratory standard for more than forty years, Methods in Enzymology is one of the most highly respected publications in the field of biochemistry. Since 1955, each volume has been eagerly awaited, frequently consulted, and praised by researchers and reviewers alike. Now with more than 300 volumes (all of them still in print), the series contains much material still relevant today--truly an essential publication for researchers in all fields of life sciences.
Specific Role of RhoC in Tumor Invasion and Metastasis
Abstract: Rho GTPases are regulators of many cellular functions and are often dysregulated in cancer. However, the precise role of Rho proteins for tumor development is not well understood. In breast cancer, overexpression of RhoC is linked with poor prognosis. Here, we aim to compare the function of RhoC and its homolog family member RhoA in breast cancer progression. We established stable breast epithelial cell lines with inducible expression of RhoA and RhoC, respectively. Moreover, we made use of Rho-activating bacterial toxins (Cytotoxic Necrotizing Factors) to stimulate the endogenous pool of Rho GTPases in benign breast epithelial cells and simultaneously knocked down specific Rho pro...
