Voltage-gated Ca2+ channels : pharmacology, modulation and their role in human disease
Author(s)
Bibliographic Information
Voltage-gated Ca2+ channels : pharmacology, modulation and their role in human disease
（Handbook of experimental pharmacology, 279）
Springer, c2023
Available at / 3 libraries
-
No Libraries matched.
- Remove all filters.
Description and Table of Contents
Description
The aim of this volume is to summarize novel findings on the function, pathophysiology, and regulation of voltage-gated Ca2+ channels and on novel concepts of their pharmacological modulation. Impressive insights into the role of channel function and regulation have come from Ca2+ channelopathies affecting the pore-forming as well as accessory subunits and channel-interacting proteins. Moreover, the long-sought molecular basis for key regulatory pathways have been discovered as well as exciting concepts of their subtype-selective pharmacological modulation.
Table of Contents
Preface.- Part 1 Modulation.- Cav1.1Calcium Channel Signaling Complexes in Excitation-Contraction Coupling: Insights from Channelopathies.- Mechanisms of Vascular CaV1.2 Channel Regulation During Diabetic Hyperglycemia.- Sympathetic Nervous System Regulation of Cardiac Calcium Channels.- Modulation of CaV1.2 Channel Function by Interacting Proteins and Post-Translational Modifications: Implications in Cardiovascular Diseases and COVID-19.- Part 2 Pharmacological Approaches.- Pathophysiological Roles of Auxiliary Calcium Channel 2 Subunits.- Design and Applications of Genetically-Encoded Voltage-Dependent Calcium Channel Inhibitors.- Part 3 Disease insight from channelopathies: consequences for pharmacology and therapeutic strategies.- CACNA1C-Related Channelopathies.- CACNA1D-Related Channelopathies: From Hypertension to Autism.- CACNA1A-Related Channelopathies: Clinical Manifestations and Treatment Options.- CaV3.2 (CACNA1H) in Primary Aldosteronism,- CaV3.3 Channelopathies.- Pathophysiological Roles of Auxiliary Calcium Channel 2 Subunits.
by "Nielsen BookData"
