Related Experiment Video
Updated: Apr 12, 2026

Controllable Ion Channel Expression through Inducible Transient Transfection
Published on: February 17, 2017
Cold-Inducible RNA-Binding Protein Regulates Cardiac Repolarization by Targeting Transient Outward Potassium Channels
Jun Li1, Duanyang Xie1, Jian Huang1
1From the Key Laboratory of Arrhythmias of the Ministry of Education of China, East Hospital, Tongji University School of Medicine (J.L., D.X., J.H., F.L., D.S., Y.L., L.L., L.G., Y.W., D.L., Y.-H.C.); Institute of Medical Genetics, Tongji University (J.L., D.S., Y.L., L.L., D.L., Y.-H.C.); Research Center for Translational Medicine, East Hospital, Tongji University School of Medicine (J.L., D.S., Y.L., L.L., D.L., Y.-H.C.); Department of Cardiology, East Hospital, Tongji University School of Medicine (D.X., J.H., F.L., L.G., Y.W., Y.-H.C.) and Department of Pathology and Pathophysiology, Tongji University School of Medicine, Shanghai, China (Y.-H.C.).
Rationale:
Cold-inducible RNA-binding protein (CIRP) is constitutively expressed at low levels across various tissues. It is rapidly upregulated by multiple stresses, underlying a general role for CIRP in organic adaptations to pathophysiological conditions. However, the role of CIRP in the heart remains unclear.
Objective:
To examine the biofunctions of CIRP in the mammalian heart.
Methods And Results:
Rats with targeted disruption of Cirp were generated using the TALEN (transcription activator-like effector nucleases)-based genome editing technique. The Cirp-knockout rats had structurally and functionally normal hearts. Resting ECG recordings revealed a short rate-corrected QT (QTc) interval in Cirp-null rats without any abnormalities in PR interval, RR interval or QRS waves as compared to wild-type animals. The shortened QTc interval from Cirp ablation was tightly linked to an abbreviated action potential duration in cardiac myocytes, which was attributable to increased transient outward potassium current (Ito). Furthermore, our findings uncovered that CIRP protein selectively bonded to KCND2 and KCND3 mRNAs encoding the functional α-subunits of Ito channel proteins. CIRP deficiency did not change the transcriptional activity of KCND2 or KCND3, but it facilitated their translation. Cirp knockout had no effect on the functional expression of ion channels other than Ito channels.
Conclusions:
CIRP modulates cardiac repolarization by negatively adjusting the expression and function of Ito channels. Our study may open a window to decipher the potential function of RNA-binding proteins in bioelectric activity.
More Related Videos
09:36Dual-Dye Optical Mapping of Hearts from RyR2R2474S Knock-In Mice of Catecholaminergic Polymorphic Ventricular Tachycardia
Published on: December 22, 2023
10:20Method for Identifying Small Molecule Inhibitors of the Protein-protein Interaction Between HCN1 and TRIP8b
Published on: November 11, 2016
Related Concept Videos
G-Protein Gated Ion Channels
Sensory...
Cardiac Action Potential
The cardiac action potential process involves a series of phases characterized by the movement of ions across the cardiac cell membranes, leading to the depolarization and repolarization of the cardiac myocytes.
Ionic Basis of Cardiac Action Potentials
Mechanism of Cardiac Arrhythmias
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers
Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Regulation of the Unfolded Protein Response