Titlebook: GTPase Protocols; The Ras Superfamily Ed Manser,Thomas Leung Book 2002 Humana Press 2002

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Using cDNA-Representational Difference Analysis (cDNA-RDA) in Combination with Microarrays to Identi diphosphate (GDP)-bound state. They integrate signals from the cell surface to the nucleus, regulating important cellular activities. For example, Ras itself is activated when extracellular growth factors such as platelet derived growth factor (PDGF) or epidermal growth facor (EGF) bind to their re

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Ras and Rac as Activators of Reactive Oxygen Species (ROS)enced a recent surge in interest. Known to cause DNA damage, and implicated in disease processes as wide-ranging as atherosclerosis and kidney disease, ROS have appeared in unlikely capacities within the Ras signaling pathway. Eschewing their evil ways, ROS have been shown to be essential for mitoge

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Interfering with Ras Signaling Using Membrane-Permeable Peptides or Drugsne (proto-oncogene) encoding a Tyr kinase called c-Src in early 1980s, it was firmly established that the malignant transformation of normal cells is caused by a combination of the following genetic events: overexpression of a protooncogene or constitutive activation of its gene product (mitogenic s

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A Ras-Based Module to Generate 32P-Labeled Fusion Proteins for Blot Overlaysid screening. Of these, the blot overlay protocol of sodium dodecyl sulfate (SDS)-acrylamide-gel-separated proteins provides perhaps the most direct assessment of target binding, since one can simultaneously screen multiple cell types or tissue extracts, and infer the size-and in some cases the rela

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Cell Motility and Invasion Assaysmune function. Deregulated motile behavior is believed to contribute to pathological processes such as metastasis, tumor angiogenesis, and atherosclerosis (.–.). Rho family members control a multitude of functions that have been implicated in the regulation of cell migration. Most notable among thes

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Isolation of Regulatory Proteins for the Rab3 Subfamily GTPasesosis, and transcytosis (.–.). All the Rab GTPases have unique C-terminal structures, which undergo posttranslational modifications with geranylgeranyl moieties in most cases. Rab GTPases cycle between the guanosine diphosphate (GDP)-bound inactive and guanosine triphosphate (GTP)-bound active forms