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G-Protein Gated Ion Channels

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...

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Related Experiment Video

Updated: Jan 12, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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Published on: June 3, 2018

FGF13 Regulates VGSC-Independent Cardiomyocyte Impulse Propagation via Cx43 Trafficking.

Lala Tanmoy Das^1,2, Mattia Malvezzi^2,3, Aravind Gade²

¹Tri-Institutional Weill Cornell/Rockefeller/Sloan Kettering Medical Scientist Training Program, New York, NY (L.T.D.).

Circulation Research

|November 7, 2025

Summary

Fibroblast growth factor homologous factor 13 (FGF13) regulates cardiac Cx43 trafficking and microtubule stability, impacting heart electrical conduction independently of voltage-gated sodium channels.

Keywords:

connexin 43 fibroblast growth factor mice, knockout mice, transgenic myocytes, cardiac

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Published on: November 13, 2015

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Last Updated: Jan 12, 2026

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Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

Published on: November 13, 2015

Area of Science:

Cardiovascular Biology
Molecular Cardiology
Ion Channel Physiology

Background:

Fibroblast growth factor homologous factors (FHFs) are linked to arrhythmias.
While FHFs regulate voltage-gated sodium channels (VGSCs), their non-VGSC roles, particularly with connexin 43 (Cx43) gap junctions, are less understood.

Purpose of the Study:

To investigate the role of FGF13 in cardiac conduction and Cx43 regulation.
To elucidate the mechanisms underlying FGF13's effects on cardiomyocyte function.

Main Methods:

Cardiac-specific Fgf13 ablation in mice (c Fgf13 KO).
Pharmacological targeting of Cx43 gap junctions and hemichannels.
Proximity labeling proteomics to identify FGF13 interaction partners.
Microscopy and optical mapping to assess Cx43 trafficking and cardiac conduction.

Main Results:

FGF13 ablation prolonged QRS and QT intervals, decreased conduction velocity, and depolarized resting membrane potential.
Cx43 trafficking was perturbed, with reduced intercalated disc localization and increased hemichannel activity.
FGF13's effects were independent of VGSCs and involved regulation of microtubule-dependent transport.

Conclusions:

FGF13 is crucial for proper Cx43 trafficking and cardiac impulse propagation.
FGF13 regulates cardiac function through microtubule-dependent mechanisms impacting Cx43, independent of VGSCs.