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March 29, 2011The Journal of PhysiologyOpen Access

Ca2+–calmodulin‐dependent protein kinase II represses cardiac transcription of the L‐type calcium channel α1C‐subunit gene (Cacna1c) by DREAM translocation

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Population

Cardiomyocytes (preclinical model)

Comparison

Overexpression of cytosolic or nuclear CaMKII… vs Control cardiomyocytes

Design

Preclinical

Key result

CaMKII downregulates the expression of the L-type calcium channel Cav1.2 subunit by potentiating the calcium-induced nuclear translocation of the transcriptional repressor DREAM.

Authors

JRJarkko RonkainenSHSandra L. HänninenTKTopi Korhonen

Discussion

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Overview

May inform experimental calcium regulation in cardiomyocytes; leaves open translation to human cardiac disease.

Structured PICO

P
Population
Cardiomyocytes (preclinical model)
I
Intervention
Overexpression of cytosolic (δC) or nuclear (δB) CaMKII isoforms, and pharmacological inhibition of CaMKII activity
C
Comparator
Control cardiomyocytes
O
Outcome
Expression of the pore-forming α-subunit (Cav1.2) of the L-type calcium channel (LTCC) and DREAM nuclear translocationsurrogate

CaMKII downregulates L-type calcium channel expression via DREAM translocation, constituting a physiological feedback mechanism to adjust calcium influx in cardiomyocytes.

Cite This Study

Ronkainen et al. (2011) studied this question. CaMKII overexpression or inhibition was evaluated on Expression of Cav1.2 and LTCC current density. CaMKII downregulates the expression of the L-type calcium channel Cav1.2 subunit by potentiating the calcium-induced nuclear translocation of the transcriptional repressor DREAM.

synapsesocial.com/papers/6a0d2e4a48a82a5ce309a832https://doi.org/10.1113/jphysiol.2010.201400
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