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"The principal focus of Mechanisms and Consequences of Proton Transport is on the gastric parietal cell and the acid secretory apparatus: how it operates and the consequences of malfunction.
Key topics include: - the fundamental structure and molecular operation of the gastric H+/K+ exchange pump;
- gene targeting studies directed at functional changes in the gastric epithelium and its ability to deal with the pathological consequences of acid and Helicobacter pylori infection; and
- regulation of parietal cell activation by protein kinases and ion transport pathways; the parietal cell as a model to study mechanisms for the translocation, docking, and fusion of membranes associated with regulated recruitment and recycling of transport proteins.This book provides cutting edge research for physiologists, cell biologists, and gastroenterologists who wish to understand the mechanisms of the gastric proton pump and the consequences of malfunction and pathology. "
Sommario
Preface. Structure and Function of H,K-ATPASE - Molecular Basis for Drug Targets. 1. The Gastric H,K-ATPase; O. Vagin, et al. 2. Human Nongastric H,K-ATPase: Current View On Structure and Functional Properties; G. Adams, et al. 3. Functional Consequences of Subunit Interactions in Na,K- and H,K-ATPases; G. Crambert, et al. 4. HKcalpha Encodes Ouabain-Insensitive H,K-ATPase in Surface Cells of Rat Distal Colon; H.J. Binder. 5. Molecular Diversity and Regulatory Heterogeneity of H,K-ATPases in Kidney; T.D. Dubose, et al. 6. Mutational Analysis of Gastric Proton Pump, alpha- and beta-Subunits; S. Asano, et al. 7. Structure-Activity Relationships of Na,K-ATPase, and H,K-ATPase; J.J.H.H.M. de Pont, et al. 8. The Effect of Mutations Within a Cluster of Homologous Amino Acids Present in the M5, M6 and M8 Transmembrane Regions of the H,K-ATPase; E.C. Rabon, et al. 9. Host-Specific H. pylori Inhibition of H,K-ATPase alpha Subunit Gene Expression; A. Smolka, M. Göõz. 10. H+,K+-ATPase, the Dominant Gastric Autoantigen In Helicobacter pylori Infection; B.J. Appelmelk, et al. 11. The Gastric H/K ATPase in the Pathogenesis of Autoimmune Gastritis; B.-H. Toh, et al. 12. Duodenal Protection: Influence of Melatonin and Other Intestinal Transmitters on Duodenal Bicarbonate Secretion and Enterocyte Signaling; G. Flemström, M. Sjöblom. 13. Role of Cytokines in Helicobacter pylori-Induced Gastric Epithelial Cell Matrix Metalloproteinase Secretion and Activation; M. Gööz, et al. 14. HCl Causes Less Intracellular A
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Tetsuro Urushidani is an associate professor in the Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, The University of Tokyo.
John G. Forte is a professor in the Department of Molecular and Cell Biology, University of California at Berkeley.
George Sachs is Director of the Membrane Biology Laboratory, University of California, Los Angeles, Professor of Physiology and Medicine, UCLA, Wilshire Chair in Medicine, UCLA, and Co-Director of the Center for Ulcer Research and Education, UCLA.
Riassunto
This volume represents the proceedings of the 9th International Proton Transport Conference, "Mechanisms and Consequences of Proton Transport" held in Leura, Australia, August 19 -21, 200 I. This conference has been held since 1971 every 3 to 4 years with few exceptions in association with the Congress of the International Union of Physiological Sciences. The first meeting was held in Frankfurt, Germany, at the Max-Planck'Institute. Countries hosting the conference have been Germany (twice), Sweden (twice), India, Canada, USA, Great Britain, and now Australia. Over the past 30 years participants at these Proton Transport Conferences have been principal contributors to the major discoveries in the physiology, biochemistry and pharmacology of gastric acid secretion. These include development of the H2-receptor blockers, defining the signaling pathways for the regulation of acid secretion, identifying the gastric proton pump, discovery and development of proton pump inhibitory drugs, and elucidating the physiology and biochemistry of Helicobacter pylori.
