
Calcium Signals
Description
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Calcium is essential for life, and a rise in cytosolic free calcium (Ca2+) in a vast majority of cell types is interpreted as a key cellular signal. Written by expert contributors, this much-needed book emphasizes a quantitative and comprehensive perspective to explore the many dimensions of cellular Ca2+ signalling. Leading researchers in the field of calcium signaling present key aspects of this process in cells, starting with Ca2+ entry into the cell, its uptake from the cytosol by organelles, such as the endoplasmic reticulum and mitochondria, and the actions of Ca2+ in turn on a variety of important cellular regulatory processes. Each chapter expertly describes the development of new techniques to study Ca2+ alongside the new concepts that the field of calcium signaling has heavily relied upon. In addition, to demonstrate the wide scope of calcium research, selected chapters describe calcium signaling in a variety of cell types, including endocrine cells, muscle, neurons and additional cell types. This research and reference text should prove useful to a wide readership, from students to researchers at many different levels, particularly in physiology, pharmacology, or biomedical engineering.
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Persons
Dr Leslie S. Satin is the Joanne I. Moore Endowed Research Professor of Pharmacology of the University of Michigan Medical School. He obtained his PhD from UCLA in the laboratory of D. Junge and conducted postdoctoral work at Stony Brook University with P. R. Adams and at the University of Washington, Seattle, with D. Cook. His research has focused on calcium signaling, ion channels, oscillations, and stimulus-secretion coupling in pancreatic beta cells.
Manu Ben-Johny is an Assistant Professor in the Department of Physiology and Cellular Biophysics at Columbia University. He received a BS in Biomedical Engineering and Mathematics from Saint Louis University, and subsequently completed his PhD in Biomedical Engineering at Johns Hopkins University under the tutelage of David Yue. His lab focuses on the biophysics and physiology of voltage-gated sodium and calcium ion channels that shape cardiac and neuronal action potentials and in developing nature-inspired approaches to manipulate ion channel function.
Ivy Dick is an assistant professor in the Physiology Department at the University of Maryland, School of Medicine. She began her career under the direction of Drs. Charles Cohen and Owen McManus at Merck Research Labs and subsequently earned her doctoral degree under the direction of Dr. David Yue in the Biomedical Engineering department at Johns Hopkins University, where she studied the mechanisms underlying calmodulin regulation of voltage-gated calcium channels. Dr. Dick's current research focuses on understanding the mechanisms of voltage-gated calcium channel regulation, and how genetic mutations disrupt channel function.
Content
Preface
Acknowledgement
Editor Biographies
List of contributors
1. Introduction
Part I Molecules mediating calcium influx
2. Calcium channel selectivity and permeation: function meets 3D structure
3. Structure and function of TRP channels
4. Glutamate-gated calcium currents in the central nervous system: structural determinants, regulatory mechanisms, and biological functions
Part II Calcium signaling on channels and other effectors
5. Monitoring the dynamics of calcium signaling effectors using genetically encoded fluorescent biosensors
6. Calcium-activated potassium channels
7. Calcium-activated chloride channels
Part III Physiological roles of calcium
8. Excitation-contraction coupling in skeletal muscle: fast Ca2+ signaling for muscle activation
9. Voltage-gated Ca2+ channels and excitation-secretion coupling at the synapse
10. Calcium signaling in context: case studies in endocrine cells
Part IV Calium channels in organelles
11. Characterization of endo-lysosomal cation channels using calcium imaging
12. The structural era of the mitochondrial calcium uniporter
Part V
13. Voltage-gated calcium channelopathies
14. Role of dysregulated calcium in neuropsychiatric diseases
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