Big on Bk: Current Insights into the Function of Large Conductance Voltage- and Ca2+- Activated K+ Channels at the Molecular, Cellular and Systemic Levels

 
 
Academic Press
  • 1. Auflage
  • |
  • erschienen am 26. Mai 2016
  • |
  • 550 Seiten
 
E-Book | ePUB mit Adobe DRM | Systemvoraussetzungen
E-Book | PDF mit Adobe DRM | Systemvoraussetzungen
978-0-12-803647-1 (ISBN)
 

Big on Bk: Current Insights into the Function of Large Conductance Voltage- and Ca2+- Activated K+ Channels at the Molecular, Cellular and Systemic Levels, a volume in the International Review of Neurobiology series, is a comprehensive overview of the state-of-the-art research into this area. It reviews current knowledge and understanding, and also provides a starting point for researchers and practitioners entering the field.


  • The latest volume in the International Review of Neurobiology series
  • Provides a broad coverage of subject matter at the molecular, cellular and systemic levels
  • Presents an ideal resource for researchers and practitioners, and those just entering the field
0074-7742
  • Englisch
  • San Diego
  • |
  • USA
Elsevier Science
  • 11,53 MB
978-0-12-803647-1 (9780128036471)
0128036478 (0128036478)
weitere Ausgaben werden ermittelt
  • Front Cover
  • Big on BK: Current Insights into the Function of Large Conductance Voltage- and Ca2+-Activated K+ Channels at the Molecular ...
  • Copyright
  • Contents
  • Contributors
  • Preface
  • Chapter One: Biophysics of BK Channel Gating
  • 1. Introduction
  • 2. Voltage-Dependent Gating in BK Channels
  • 2.1. Our Current Understanding of Voltage-Dependent Channel Gating
  • 2.2. Operation of the Noncanonical BK Channel VSD
  • 2.3. Modulation of BK Voltage-Dependent Gating
  • 3. Ligand-Dependent Gating in BK Channels
  • 3.1. Ca2+-Dependent Gating
  • 3.2. Mg2+-Dependent Gating
  • 4. The BK Allosteric Gating Mechanism
  • 4.1. The HCA and HA Models of Allosteric BK Channel Activation
  • 4.2. Electromechanical Coupling
  • 4.3. Modulation of Electromechanical Coupling
  • 4.4. Coupling Between the Ca2+ Sensors and the Gate
  • 4.5. Modulation of BK Ca2+ Sensitivity
  • 4.6. Coupling Between Voltage and Ca2+ Sensors
  • 4.7. Coupling Between RCK1 and RCK2 Ca2+ Sensors
  • 5. The Extraordinary Conductance of BK Channels
  • 6. Concluding Remarks: The BK Channel as a Rebel and a Model
  • Acknowledgments
  • References
  • Chapter Two: Modulation of BK Channel Function by Auxiliary Beta and Gamma Subunits
  • 1. Introduction
  • 2. Discovery
  • 3. Structural Characteristics
  • 4. Modulation of the BK Channel´s Biophysical Properties by ß Subunits
  • 5. Modulation of the BK Channel´s Biophysical Properties by ? Subunits
  • 6. Modulation of the BK Channel´s Pharmacological Properties by ß and ? Subunits
  • 7. Stoichiometry
  • 8. Physiological and Pathological Relevance or Roles
  • 9. Perspectives
  • Acknowledgment
  • References
  • Chapter Three: Posttranscriptional and Posttranslational Regulation of BK Channels
  • 1. Introduction
  • 1.1. Spatiotemporal Control of BK Channel Number and Activity
  • 2. Posttranscriptional Regulation
  • 2.1. Alternative Pre-mRNA Splicing
  • 2.1.1. Control of Alternative Splicing of the Pore-Forming a-Subunit
  • 2.1.2. Alternative Splicing Controls the Biophysical Properties of BK Channels and Their Regulation by PTMs, Accessory Su ...
  • 2.1.3. Splicing and Control of BK Channel Trafficking
  • 2.1.4. Splicing and the Control of Regulatory ß-Subunits
  • 2.2. miRNA Control of Abundance and Diversity
  • 2.3. RNA Editing
  • 3. Posttranslational Modification
  • 3.1. Reversible Protein Phosphorylation
  • 3.1.1. Regulation by Reversible Serine-Threonine Protein Phosphorylation
  • 3.1.1.1. Control of Channel Activity via Regulation of Pore-Forming a-Subunits
  • 3.1.1.2. Control of Regulatory Subunits by Serine/Threonine Phosphorylation
  • 3.1.1.3. Control of Channel Trafficking
  • 3.1.1.4. Protein Serine/Threonine Dephosphorylation
  • 3.1.2. Reversible Tyrosine Phosphorylation
  • 3.2. Lipidation
  • 3.2.1. Reversible S-Acylation
  • 3.2.2. Atypical Internal Protein Myristoylation
  • 3.3. N-Linked Glycosylation
  • 3.4. Ubiquitination
  • 4. Conclusions and Perspectives
  • Acknowledgments
  • References
  • Chapter Four: Protein Network Interacting with BK Channels
  • 1. Introduction
  • 2. Calcium Channels that Functionally Couple with BK Channels
  • 2.1. Voltage-Gated Calcium Channels
  • 2.2. Other Calcium Channels
  • 3. Actin Cytoskeleton
  • 3.1. Actin
  • 3.2. Synaptopodin
  • 3.3. Filamin A
  • 4. Targeting/Trafficking of BK Channels to the Plasma Membrane
  • 4.1. Membrane-Associated Guanylate Kinase with Inverted Orientation Protein 1
  • 4.2. a-Tubulin and Microtubule-Associated Protein 1A
  • 4.3. Trafficking from the Endoplasmic Reticulum: Cereblon
  • 5. Proteins that Affect the Localization of BK Channels to Specific Plasma Membrane Compartments
  • 5.1. ß-Catenin
  • 5.2. Caveolins
  • 5.3. Syntaxin-1A
  • 5.4. a-Catulin and the Dystrophin Complex
  • 6. Proteins that Mediate the Removal or Degradation of BK Channels: Dynamin-1
  • 7. Proteins that Alter Channel Function
  • 7.1. Cortical Actin Binding Protein
  • 7.2. Ankyrin Repeat Family A
  • 7.3. Protein Kinases and Phosphatases
  • 7.4. Receptor Activated C Kinase 1
  • 7.5. Apolipoprotein A1
  • 8. Examples of BK Channel Interactomes
  • 8.1. Hemoxygenase 2
  • 8.2. Myelin Binding Protein
  • 8.3. Isoform-Specific-Interacting Proteins
  • 8.4. BK Channel Interactomes
  • 8.4.1. Interactome in Mouse Whole Brain
  • 8.4.2. Interactome of Synaptic Proteins
  • 8.4.3. Interactome in Cochlea
  • 9. Discussion
  • Acknowledgments
  • References
  • Chapter Five: Functional Role of Mitochondrial and Nuclear BK Channels
  • 1. Mitochondrial BK Channels
  • 1.1. Biophysical and Pharmacological Properties of mitoBK Channels
  • 1.2. mitoBK Channel Composition
  • 1.3. Function of mitoBK Channels
  • 2. Nuclear BK Channels
  • 2.1. Evidence for BK Channels in the Nucleus
  • 2.2. The Function of nBK Channels
  • 2.2.1. nBK Channels Regulate Nuclear Transmembrane Potential
  • 2.2.2. nBK Channels Regulate Nuclear Ca2+ Signals
  • 2.2.3. nBK Channels Regulate Nuclear Ca2+ Signaling and Transcription
  • 2.2.4. nBK Channels Regulate Dendritic Arborization
  • 3. Summary and Future Perspectives
  • Acknowledgments
  • References
  • Chapter Six: Modulation of BK Channels by Small Endogenous Molecules and Pharmaceutical Channel Openers
  • 1. Introduction
  • 2. Salient Features of the BK Channel
  • 3. Classification of Modulators by Their Mode of Action
  • 4. Modulation of ``N´´
  • 5. Modulation of ``i(Vm)´´
  • 6. Modulation of Open Probability
  • 7. G(Vm) Changes by Modulators with Different Modes of Action
  • 8. Intrinsic Behavior of the Ion Conduction Gate
  • 9. Voltage-Sensor Domain Function
  • 10. Coupling Between the Ion Conduction Gate and VSDs
  • 11. Ca2+ Sensors
  • 12. Coupling Between the Ion Conduction Gate and Ca2+ Sensors
  • 13. Coupling Between the VSDs and Ca2+ Sensors
  • 14. Multistep Interactions
  • 15. Modulators with Well-Characterized Mechanisms of Action
  • 16. Modulators Whose Mechanisms Can Be Inferred
  • 17. Modulators with an Unknown Mode of Action
  • 18. Structural Bases of Modulatory Action
  • 19. Importance of Mechanistic Information
  • 20. Summary and Future Outlook
  • Acknowledgments
  • References
  • Chapter Seven: Modulation of BK Channels by Ethanol
  • 1. Introduction: Is the BK Channel an Ethanol Receptor?
  • 2. Responses of Native BK Channels to Clinically Relevant Ethanol Concentrations in Ethanol-Naïve Systems
  • 3. Molecular Determinants of Changes in BK Channel Steady-State Activity Evoked by Clinically Relevant Ethanol Concentrat ...
  • 3.1. Activating Ions
  • 3.2. Slo1 Protein Isoforms
  • 3.3. Channel Regulatory ß Subunits
  • 3.4. Posttranslational Modifications of BK Subunits
  • 3.5. Lipid Microenvironment of the BK Channel Complex
  • 4. Adaptations in BK Channel/Coding Genes to Protracted or Repeated Ethanol Exposure: From Molecular Mechanisms to Modifi ...
  • 5. Conclusions
  • Acknowledgment
  • References
  • Chapter Eight: BK Channels in the Central Nervous System
  • 1. Overview
  • 2. Expression Patterns of BK Channel Subunits in the CNS
  • 2.1. Pore-Forming Subunit (a)
  • 2.1.1. Localization
  • 2.1.2. Ontogeny
  • 2.2. Auxiliary Subunits (ß and ?)
  • 2.2.1. Localization
  • 2.2.2. Functional Signatures
  • 2.3. Subcellular Trafficking
  • 3. Role of BK Channels in CNS Cellular Physiology
  • 3.1. Neurons
  • 3.1.1. Calcium Nanodomains
  • 3.1.2. Regulation of Neural Firing
  • 3.1.3. Regulation of Neurotransmitter Release
  • 3.1.4. Regulation of Dendritic Excitability
  • 3.2. Astrocytes
  • 3.3. Microglia
  • 3.4. Other Cell Types
  • 4. Role of BK Channels in CNS Function and Pathologies
  • 4.1. Control of the Circadian Rhythm
  • 4.2. Epilepsy
  • 4.3. Movement Disorders
  • 4.4. Cerebral Ischemia
  • 4.5. Alzheimer´s Disease
  • 4.6. Adult-Onset Neuronal Ceroid Lipofuscinosis
  • 4.7. Mental Retardation
  • 4.8. Alcohol Use Disorders
  • 4.9. Pain
  • 4.10. In the Eye
  • 5. Conclusions
  • Acknowledgments
  • References
  • Chapter Nine: BK Channels and the Control of the Pituitary
  • 1. Overview and Anatomy of the Pituitary Gland
  • 1.1. Introduction
  • 1.2. Pituitary Anatomy and Systems
  • 1.3. Identification of Pituitary Cell Types
  • 2. Electrical Excitability of Anterior Pituitary Cells
  • 2.1. Pituitary Cell Excitability Is Different Compared to Neurons
  • 3. Paradoxical Role of BK Channels and Bursting
  • 3.1. BK Channels in the Anterior Pituitary
  • 3.2. Experimental Investigation of BK Channels and Bursting in Corticotrophs
  • 3.3. Modeling the Role of BK Channels on Pituitary Cell Excitability
  • 3.4. Properties and Molecular Identification of BK Channels Controlling Bursting
  • 4. BK Channels in Hypothalamic Neurons Regulating the Pituitary
  • 4.1. Magnocellular and Parvocellular Neurosecretory Cells
  • 5. Aims and Challenges for Understanding the Role of BK Channels in the Pituitary
  • 5.1. Anterior Pituitary Cell Excitability in Networks
  • 5.2. Pharmacological Tools for Investigating Pituitary Excitability
  • 5.3. Dynamic Clamp Integrates Modeling and Experimentation
  • 5.4. Conclusions
  • Acknowledgments
  • References
  • Chapter Ten: BK Channels in the Vertebrate Inner Ear
  • 1. Introduction to the Auditory Periphery
  • 2. BK Channel Structure and Function in Nonmammalian Auditory Organs
  • 2.1. Electrical Tuning of Nonmammalian Hair Cells
  • 2.2. Interplay of BK Channels and VGCCs
  • 2.3. Tonotopic Distribution of BK Channel Properties
  • 2.4. Splice Variation
  • 2.5. Regulatory ß Subunits
  • 2.6. Other Possibilities
  • 3. BK Channels in the Mammalian Cochlea
  • 3.1. Anatomy of the Mammalian Auditory Sensory Epithelium
  • 3.2. BK Channel Expression in the Mammalian Auditory Sensory Epithelium
  • 3.2.1. Inner Hair Cells
  • 3.2.2. Outer Hair Cells
  • 3.2.3. Spiral Ganglion Neurons
  • 3.2.4. Efferent Terminals
  • 3.3. Function of BK Channels in the Mammalian Auditory System
  • 3.3.1. Maturation of the Auditory System
  • 3.3.2. Afferent Synaptic Transmission
  • 3.3.3. Protection from Acoustic Overexposure
  • 3.3.4. High-Frequency Hearing
  • 3.4. BK Channels in Vestibular Hair Cells
  • 4. Conclusion
  • References
  • Chapter Eleven: BK Channels in the Vascular System
  • 1. Introduction
  • 1.1. Peripheral Vascular Resistance and Autoregulation of Blood Flow
  • 1.2. Vascular Wall Structure: Form Determines Function
  • 1.3. Myogenic Response for the Autoregulation of Blood Flow
  • 1.4. The SMC as the Determinant of the Myogenic State
  • 2. BK Channels in Vascular Smooth Muscle
  • 2.1. Ca2+ Addresses the ``State of the Smooth Muscle´´
  • 2.2. The RyR/BK Complex: Think Local, Act Global
  • 2.3. IP3-Mediated Activation
  • 2.4. Endothelial BK Channels
  • 3. Vascular Regulation by BK Channels
  • 3.1. Phosphorylation
  • 3.2. Nitric Oxide
  • 3.3. Estrogen
  • 3.4. Lipid Metabolism
  • 3.4.1. Fatty Acids
  • 3.4.2. Metabolites of AA by the COX Pathway
  • 3.4.3. Metabolites of AA by the Cytochrome P450 Epoxygenase Pathway
  • 3.5. Reactive Oxygen Species
  • 4. Regulation of Neurogenic Tone by BK Channels
  • 4.1. Neurotransmitters
  • 4.2. Neurovascular Coupling
  • 5. Vascular Pathology Caused by BK Channel Dysregulation
  • 5.1. Hypertension
  • 5.2. Diabetes
  • 5.3. Therapeutic Potential for BK Channels
  • References
  • Chapter Twelve: Developing Molecular Pharmacology of BK Channels for Therapeutic Benefit
  • 1. Potential Therapeutic Benefits of Targeting BK Channels
  • 2. Issues Facing the BK Channel as a Drug Target
  • 3. Natural Product Screening as a Way to Develop Molecular Pharmacology of BK Channels
  • 4. Discovery of Small Molecule BK Channel Agonists
  • 5. Identification of Potent and Selective Small Molecule BK Channel Inhibitors
  • 6. Conclusions
  • Acknowledgments
  • References
  • Index
  • Contents of Recent Volumes
  • Back Cover

Dateiformat: EPUB
Kopierschutz: Adobe-DRM (Digital Rights Management)

Systemvoraussetzungen:

Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

Das Dateiformat EPUB ist sehr gut für Romane und Sachbücher geeignet - also für "fließenden" Text ohne komplexes Layout. Bei E-Readern oder Smartphones passt sich der Zeilen- und Seitenumbruch automatisch den kleinen Displays an. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

Weitere Informationen finden Sie in unserer E-Book Hilfe.


Dateiformat: PDF
Kopierschutz: Adobe-DRM (Digital Rights Management)

Systemvoraussetzungen:

Computer (Windows; MacOS X; Linux): Installieren Sie bereits vor dem Download die kostenlose Software Adobe Digital Editions (siehe E-Book Hilfe).

Tablet/Smartphone (Android; iOS): Installieren Sie bereits vor dem Download die kostenlose App Adobe Digital Editions (siehe E-Book Hilfe).

E-Book-Reader: Bookeen, Kobo, Pocketbook, Sony, Tolino u.v.a.m. (nicht Kindle)

Das Dateiformat PDF zeigt auf jeder Hardware eine Buchseite stets identisch an. Daher ist eine PDF auch für ein komplexes Layout geeignet, wie es bei Lehr- und Fachbüchern verwendet wird (Bilder, Tabellen, Spalten, Fußnoten). Bei kleinen Displays von E-Readern oder Smartphones sind PDF leider eher nervig, weil zu viel Scrollen notwendig ist. Mit Adobe-DRM wird hier ein "harter" Kopierschutz verwendet. Wenn die notwendigen Voraussetzungen nicht vorliegen, können Sie das E-Book leider nicht öffnen. Daher müssen Sie bereits vor dem Download Ihre Lese-Hardware vorbereiten.

Weitere Informationen finden Sie in unserer E-Book Hilfe.


Download (sofort verfügbar)

178,50 €
inkl. 19% MwSt.
Download / Einzel-Lizenz
ePUB mit Adobe DRM
siehe Systemvoraussetzungen
PDF mit Adobe DRM
siehe Systemvoraussetzungen
Hinweis: Die Auswahl des von Ihnen gewünschten Dateiformats und des Kopierschutzes erfolgt erst im System des E-Book Anbieters
E-Book bestellen

Unsere Web-Seiten verwenden Cookies. Mit der Nutzung des WebShops erklären Sie sich damit einverstanden. Mehr Informationen finden Sie in unserem Datenschutzhinweis. Ok