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Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Voltage-gated Ion Channels01:26

Voltage-gated Ion Channels

Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Voltage-gated Ion Channels01:26

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Voltage-gated ion channels are transmembrane proteins that open and close in response to changes in the membrane potential. They are present on the membranes of all electrically excitable cells such as neurons, heart, and muscle cells.
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

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Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
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Patch Clamp and Perfusion Techniques for Studying Ion Channels Expressed in Xenopus oocytes
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Bio-inspired voltage-dependent calcium channel blockers.

Tingting Yang1, Lin-Ling He, Ming Chen

  • 11] Department of Physiology and Cellular Biophysics, Columbia University, College of Physicians and Surgeons, 1150 St Nicholas Avenue, New York, New York 10032, USA [2].

Nature Communications
|October 8, 2013
PubMed
Summary

Researchers developed a new method to create genetically encoded calcium channel blockers by anchoring proteins to the cell membrane. This approach, called ChIMP, offers a versatile strategy for developing novel calcium channel inhibitors.

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Area of Science:

  • Molecular biology
  • Cellular physiology
  • Pharmacology

Background:

  • Voltage-dependent calcium channels (CaV1/CaV2) are crucial for electrical signaling in excitable cells.
  • CaV1/CaV2 channel blockers have significant biotechnological and therapeutic potential.
  • Rem, a G-protein, naturally inhibits CaV1/CaV2 channels.

Purpose of the Study:

  • To develop a general method for creating novel genetically encoded calcium channel blockers.
  • To explore the potential of anchoring cytosolic proteins to the plasma membrane for channel inhibition.
  • To investigate the extension of this method to small-molecule drug discovery.

Main Methods:

  • Anchoring diverse cytosolic proteins (CaVβ, 14-3-3, calmodulin, CaMKII) to the plasma membrane.
  • Utilizing the 'channel inactivation induced by membrane-tethering of an associated protein' (ChIMP) method.
  • Engineering FK506-binding protein into CaV1.2-α1C for rapamycin-induced inhibition.

Main Results:

  • Diverse cytosolic proteins were successfully converted into tunable calcium channel blockers via membrane tethering.
  • The ChIMP method demonstrated controllable selectivity, kinetics, and potency of channel inhibition.
  • Rapamycin-induced inhibition of CaV1.2-α1C channels was achieved through engineered protein interactions.

Conclusions:

  • A universal method (ChIMP) for developing novel genetically encoded calcium channel blockers was established.
  • The ChIMP strategy offers a versatile platform for creating calcium channel inhibitors with tailored properties.
  • This approach may be extended to develop probes for various ion channels and aid small-molecule drug discovery.