Calcium Entry Channels in Non Excitable Cells 1st Edition by Juliusz Ashot Kozak, James W Putney Jr ISBN 149875273X 9781498752732

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ISBN 10: 149875273X 
ISBN 13: 9781498752732
Author: Juliusz Ashot Kozak, James W. Putney Jr

Calcium Entry Channels in Non Excitable Cells 1st Table of contents:

1 Electrophysiological Methods for Recording CRAC and TRPV5/6 Channels
1.1 Introduction
1.2 Characteristics of Calcium Entry in Non-Excitable Cells
1.3 CRAC Channels
1.3.1 CRAC Channels in the Native Environment
1.3.2 CRAC Current–Voltage Relation
1.3.3 Current Separation
1.3.4 Perforated-Patch Recording
1.3.5 CRAC Channel Activity with Various Permeating Cations
1.3.6 CRAC Single-Channel Conductance
1.3.7 Heterologously Expressed Orai/STIM Channels
1.4 TRPV5 and TRPV6 Channels
1.4.1 Heterologously Expressed TRPV5/6
1.4.2 Endogenous TRPV5/6 Channels
1.4.3 Single-Channel Conductance
Acknowledgment
References
2 Studies of Structure–Function and Subunit Composition of Orai/STIM Channel
2.1 Introduction
2.2 STIM1
2.3 Orai
2.4 STIM1: Orai Interaction
2.5 Ion Conduction Pathway of the Orai Pore
2.6 Perspectives
Acknowledgments
References
3 Signaling ER Store Depletion to Plasma Membrane Orai Channels
3.1 Introduction
3.1.1 ER Calcium Repository
3.1.2 CRAC Current and the Underlying Players
3.1.3 SOCE Current as an Outcome of STIM–ORAI Coupling
3.2 ORAI Channel Structure
3.2.1 Calcium Binding Site
3.2.2 Pore Features Mapped by Cd2+ Block and Disulfide Cross-Linking Experiments
3.2.3 Drosophila Orai Structure
3.2.4 Pore from Outside to Inside
3.2.5 Cytoplasmic Extensions of ORAI1
3.3 Overview of STIM1 Structure
3.3.1 Ca2+ Sensing by STIM1 Luminal Domain
3.3.2 Cytoplasmic Domain of STIM1
3.3.3 ORAI-Interacting Machinery
3.4 STIM Active State
3.4.1 Activation of the Luminal Domain
3.4.2 Activation Involves Extension of STIM1 Cytoplasmic Domain
3.4.3 CC1 and the Release of ORAI1-Interacting Machinery
3.4.4 Higher-Order STIM1 Oligomerization
3.5 Activation of ORAI1 Channels by STIM1
3.5.1 Interaction of Activated STIM1 with ORAI1
3.5.2 Gating of the ORAI1 Channel
3.6 Conclusions
References
4 Modulation of Orai1 and STIM1 by Cellular Factors
4.1 Introduction
4.2 Modulators of Orai1 via Protein Interaction
4.3 Vesicular Components in Regulation of Orai1
4.4 Store-Independent Regulation of Orai1 via Protein Interaction
4.5 STIM1-Interacting Molecules at the ER–PM Junctions
4.6 Modulators of STIM1 Function
4.7 STIM1 as a Regulator for Non-CRAC Channel-Related Functions
4.8 Methods Used to Identify Interacting Partners of Orai1 and STIM1
4.9 Conclusions and Perspectives
Acknowledgments
References
5 CRAC Channels and Ca2+-Dependent Gene Expression
5.1 Introduction
5.2 Ca2+ Entry through CRAC Channels Activates Gene Expression
5.3 The Importance of Ca2+ Microdomains near Open CRAC Channels in the Regulation of Transcription
5.4 How Local Is Local?
5.5 Sensing Local Ca2+ near CRAC Channels
5.6 Parallel Processing of the CRAC Channel Ca2+ Microdomain
5.7 Caveolin-1 Differentially Regulates NFAT and c-Fos Activities
5.8 Modular Regulation by Caveolin-1
5.9 Large Bulk Ca2+ Rises and c-Fos Gene Expression
5.10 Conclusion
References
6 Function of Orai/Stim Proteins Studied in Transgenic Animal Models
6.1 Introduction
6.2 Strategies for Gene Targeting
6.2.1 Conventional Gene Targeting
6.2.2 Conditional Gene Targeting
6.2.3 Gene Trapping
6.3 Establishment of Orai/Stim-Deficient Mice at the Whole-Body Level
6.3.1 Orai1 Knockout Mouse
6.3.2 Stim1 Knockout Mouse
6.3.3 Stim2 Knockout Mouse
6.3.4 Orai1 (R93W) Knock-In (KI) Mouse
6.4 Establishment of Tissue-Specific Orai/Stim-Deficient Mouse Lines
6.4.1 Orai1 Conditional KO (cKO) Mouse
6.4.2 Stim1 Conditional KO (cKO) Mouse
6.4.3 Stim2 Conditional KO (cKO) Mouse
6.4.4 Stim1 and Stim2 Double Conditional KO Mouse
6.5 Methods to Establish Murine Embryonic Fibroblast Lines from KO Mice
6.6 Function of Orai/Stim Proteins in the Immune System
6.6.1 T Lymphocytes
6.6.2 B Lymphocytes
6.6.3 Mast Cells
6.7 Function of Orai/Stim Proteins in the Muscle
6.8 Function of Orai/Stim Proteins in the Nervous System
6.9 Concluding Remarks
Acknowledgments
References
7 Assessing the Molecular Nature of the STIM1/Orai1 Coupling Interface Using FRET Approaches
7.1 Introduction
7.2 Strategy for Quantitative FRET Measurement
7.3 FRET Measurements to Quantitate SOAR–Orai1 Interactions
7.3.1 Generation of Stable Cell Lines
7.3.2 Calibration of FRET Imaging System
7.3.3 Determination of G Constant Number
7.3.4 Data Collection
7.3.5 Data Analysis
7.4 Conclusions
References
8 Optogenetic Approaches to Control Calcium Entry in Non-Excitable Cells
8.1 Introduction
8.2 Design of Opto-CRAC Constructs
8.2.1 CRY2-Based Strategy
8.2.2 LOV2-Based Strategy
8.3 Examples of Opto-CRAC Applications
8.3.1 Light-Operated Calcium Entry
8.3.1.1 Calcium Imaging Using Fura-2 AM
8.3.1.2 Calcium Imaging with GECIs
8.3.2 Spatial Control of Calcium Signals
8.3.3 Temporal Control of Calcium Signals
8.3.4 Phototunable Ca2+-Dependent Gene Expression in T Cells
8.3.4.1 Mouse Primary T Cell Isolation and Culture In Vitro
8.3.4.2 Retroviral Packaging and Transduction
8.3.4.3 Induction of IL2 and IFN-γ Expression with Blue Light
8.3.5 NIR Light Control of Calcium Signaling In Vitro and In Vivo
8.4 Conclusions
References
9 Regulation of Orai/STIM Channels by pH
9.1 Introduction
9.2 Basic Methods
9.2.1 Cell Culture and Transfection
9.2.2 Site-Directed Mutagenesis of Orai
9.2.3 Orai/STIM Current Recording by Patch-Clamp Electrophysiology
9.2.4 Ca2+ Imaging
9.2.5 Measurement of Changes in Intracellular pH by Ratiometric pHi Imaging
9.3 Regulation of Orai/STIM Channel by Internal and External pH
9.3.1 Influence of Changes of Internal and External pH on Orai/STIM Channel Activation
9.3.2 Orai/STIM Channel Regulation by External Protons
9.3.3 Regulation of Orai/STIM Channel Activity by Internal Protons
9.3.4 Evaluation of Proton Permeation
9.4 Molecular Mechanisms of pH Sensitivity
9.4.1 Key Amino Acid Residues Responsible for Extracellular pH Sensitivity
9.4.2 Molecular Basis of Intracellular pH Sensitivity of Orai/STIM Channels
9.5 Functional Assessment of pH Regulation of Orai/STIM Channels
9.6 Summary and Future Research Directions
Acknowledgments
References
10 Non-Orai Partners of STIM Proteins
10.1 Introduction
10.2 ER–PM Ca2+ Signaling by STIM
10.3 Molecular Recognition of Non-Orai Signaling Molecules by STIM
10.3.1 Non-Orai PM Ca2+ Transport Molecules as STIM Effectors
10.3.1.1 TRPC Channels
10.3.1.2 Voltage-Gated Ca2+ Channels (CaV)
10.3.1.3 Plasma Membrane Ca2+ ATPase (PMCA) and Na+/Ca2+ Exchanger (NCX)
10.3.2 ER Proteins as Regulators and Effectors
10.3.2.1 SARAF
10.3.2.2 STIMATE
10.3.2.3 POST
10.3.2.4 Junctate
10.3.2.5 ORMDL3
10.3.2.6 ERp57
10.3.2.7 Sarco/Endoplasmic Reticulum Ca2+ ATPase (SERCA)
10.3.3 Cytoplasmic Junctional Regulators
10.3.3.1 CRACR2A
10.3.3.2 Golli
10.3.4 Microtubules
10.3.5 Membrane Lipid Domains
10.4 ER–PM Junctional Ca2+ Signaling Hub—Molecular Recognition Meets Nanoarchitecture
10.5 Conclusion and Perspectives
References
11 Store-Independent Orai Channels Regulated by STIM
11.1 Introduction
11.2 Biophysical Properties and Molecular Composition of SICE Channels
11.3 Methods for Measuring SICE Channel Function
11.3.1 Whole-Cell Patch Clamp Recording
11.3.1.1 Equipment Setup for Patch Clamp Recording
11.3.1.2 Solutions for Electrophysiological Recordings
11.3.1.3 Experimental Procedures
11.3.2 Calcium Imaging
11.3.2.1 Equipment Setup for Fluorescence Calcium Measurement
11.3.2.2 Ca2+ Indicators
11.3.2.3 Solutions
11.3.2.4 Experimental Procedures
11.4 SICE Channel Function in Health and Disease
References
12 Regulation and Role of Store-Operated Ca2+ Entry in Cellular Proliferation
12.1 Introduction
12.2 Role of Ca2+ Signals in Cellular Proliferation
12.3 Remodeling of the Ca2+-Signaling Machinery during Meiosis
12.4 SOCE Inactivation during M-Phase
12.5 Mechanisms Regulating SOCE Inactivation during M-Phase
12.6 SOCE and Cancer
12.6.1 STIM1 and Orai1 Role in Cell Progression, Proliferation, and Cell Death of Cancer Cells
12.6.2 SOCE in Cell Motility, Metastasis, and Tumor Microenvironment
12.6.3 Orai1 and STIM1 in Antitumor Immunity
References
13 TRPV5 and TRPV6 Calcium-Selective Channels
13.1 Introduction
13.2 Ca2+ Transport across Epithelia
13.3 Identification of TRPV5 and TRPV6 by Expression Cloning
13.4 Ca2+ Transport Properties Uncovered by Various Approaches
13.4.1 Functional Expression in Xenopus Oocytes
13.4.2 Characterization of TRPV5 and TRPV6 at the Macroscopic Level
13.4.3 Characterization of TRPV5 and TRPV6 by Patch Clamping
13.4.4 Feedback Control Mechanisms
13.4.5 Ca2+ Imaging
13.4.6 Additional Experimental Considerations
13.4.7 Crystal Structure of Rat TRPV6
13.5 Physiological Roles Revealed Using Genetically Engineered Animal Models
13.5.1 TRPV5 and TRPV6 in Ca2+ Absorption and Reabsorption
13.5.2 TRPV6 as a Central Component in Vitamin D–Regulated Active Ca2+ Absorption
13.5.3 Role of TRPV6 in Maternal–Fetal Ca2+ Transport
13.5.4 Role of TRPV6 in Male Fertility
13.6 Proteins That Regulate TRPV5 and TRPV6
13.6.1 Proteins That Interact with TRPV5 and TRPV6
13.6.2 Proteins That Are Physiologically Relevant to TRPV5 and TRPV6
13.7 Potential Use of TRPV6 in Therapy and Development of Chemical Modulators
13.7.1 Evaluation of TRPV6 as a Therapeutic Target
13.7.1.1 TRPV6 in Prostate and Breast Cancer
13.7.2 Development of Chemical Modulators of TRPV6
13.7.2.1 Development of Antiproliferative Compound TH-1177
13.7.2.2 Development of TRPV6 Inhibitor “Compound #03”
13.7.2.3 Effects of Estrogen-Receptor Blocker Tamoxifen on TRPV6 Function
13.7.2.4 Ligand-Based Virtual Screening (LBVS) to Develop Improved TRPV6 Inhibitors
13.7.2.5 Analogs of 2-Aminoethyl Diphenylborinate (2-APB) as Potential Modulators of TRPV6 Function
13.8 TRPV5 and TRPV6 Mutations and Kidney Stone Diseases
13.9 Concluding Remarks
Acknowledgments
References
14 Determining the Crystal Structure of TRPV6
14.1 Introduction
14.2 Precrystallization Screening of Protein Expression and Biochemical Behavior Using FSEC
14.3 Large-Scale Purification and Crystallization
14.4 Collection and Processing of Diffraction Data
14.5 Protein Engineering to Improve Crystal Packing
14.6 Comparison of TRPV6 and Orai Structures
Acknowledgments
References
15 Identifying TRP Channel Subunit Stoichiometry Using Combined Single Channel Single Molecule Determinations (SC-SMD)
15.1 Introduction
15.1.1 Methods for the Determination of Channel Stoichiometry
15.1.2 Single Molecule Detection (SMD)
15.1.2.1 Limitations of SMD Studies
15.2 Materials
15.2.1 Cell Culture and Transient Transfection
15.2.2 Patch Clamp Electrophysiology
15.3 Methods
15.3.1 Phosphate-Buffered Saline
15.3.2 Trypsin-EDTA (0.2% Trypsin, 0.5 M EDTA pH 8.0)
15.3.3 Polyethylenimine (PEI) Solution 1 μg/μL
15.3.4 Trypsin-EDTA Treatment for Lifting of HEK-293 Cells
15.3.5 Transfecting Cells with Plasmids
15.3.6 Pipette Preparation
15.3.6.1 Checking Pipette Autofluorescence
15.3.6.2 Filling the Patch Pipette with Buffer
15.3.6.3 Mounting the SC-SMD System
15.3.6.4 Checking Pipette Resistance
15.3.6.5 Obtaining a Gigaohm Seal
15.3.6.6 Simultaneous Recording of Single-Channel Activity and Single Molecule Determinations
15.3.6.7 SMD Analysis
15.4 Conclusions
15.5 Notes
References
16 Pharmacology of Store-Operated Calcium Entry Channels
16.1 Introduction
16.2 PLC Activation and Store-Operated Calcium Channels
16.3 Pharmacological Activation of Store-Operated Channels
16.3.1 SERCA Pump Inhibition
16.3.2 Ca2+ Ionophores
16.3.3 Activation of IP3 Receptors
16.3.4 Passive Depletion of ER Ca2+ Pools
16.3.5 Membrane Potential
16.4 Pharmacological Inhibition of Store-Operated Channels
16.4.1 Lanthanides
16.4.2 2-APB (2-Aminoethyldiphenyl Borate)
16.4.3 ML-9
16.4.4 BTP2 (YM-58483)
16.4.5 Synta 66
16.4.6 GSK-7975A and GSK-5503A
16.4.7 RO2959
16.4.8 AnCoA4
16.4.9 SKF96365 and Other Imidazoles
16.4.10 Diethylstilbestrol
16.5 Concluding Remarks

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Tags: Juliusz Ashot Kozak, James W Putney Jr, Calcium Entry, Non Excitable Cells