ArticleCirculation research2006
Mitogen-activated protein kinases control cardiac KChIP2 gene expression.
Article in Circulation research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- KCells · 2023Review
- How CaThe Journal of general physiology · 2019Article
- Prominent differences in left ventricular performance and myocardial properties between right ventricular and left ventricular-based pacing modes in rats.Scientific reports · 2017Article
- Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB.The Journal of biological chemistry · 2016Article
- Effects of C-reactive protein on K(+) channel interaction protein 2 in cardiomyocytes.American journal of translational research · 2015Article
- The potential role of Kv4.3 K+ channel in heart hypertrophy.Channels (Austin, Tex.) · 2014Review
- Development of heart failure is independent of K+ channel-interacting protein 2 expression.The Journal of physiology · 2013Article
- Endothelin-1 stimulates the expression of L-type Ca2+ channels in neonatal rat cardiomyocytes via the extracellular signal-regulated kinase 1/2 pathway.The Journal of membrane biology · 2013Article
- Article
- KCNE2 protein is more abundant in ventricles than in atria and can accelerate hERG protein degradation in a phosphorylation-dependent manner.American journal of physiology. Heart and circulatory physiology · 2012Article
- KChIP2 attenuates cardiac hypertrophy through regulation of Ito and intracellular calcium signaling.Journal of molecular and cellular cardiology · 2010Article
- Long-term fish oil supplementation induces cardiac electrical remodeling by changing channel protein expression in the rabbit model.PloS one · 2010Article
- Larger transient outward K(+) current and shorter action potential duration in Galpha(11) mutant mice.Pflugers Archiv : European journal of physiology · 2010Article
- Molecular determinants of cardiac transient outward potassium current (I(to)) expression and regulation.Journal of molecular and cellular cardiology · 2010Review
- Reactive oxygen species-induced activation of p90 ribosomal S6 kinase prolongs cardiac repolarization through inhibiting outward K+ channel activity.Circulation research · 2008Article
- Regulation of Kv4 channel expression in failing rat heart by the thioredoxin system.American journal of physiology. Heart and circulatory physiology · 2008Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
Hypertrophied myocardium is associated with reductions in the transient outward K(+) current (Ito) and expression of pore-forming Kv4.2/4.3 and auxiliary KChIP2 subunits. Here we show that KChIP2 mRNA and protein levels are dramatically decreased to 10% to 30% of control levels in the left ventricle of aorta-constricted rats in vivo and phenylephrine (PE)-treated myocytes in vitro. PE also markedly decreases Ito density. Inhibition of protein kinase Cs (PKCs) does not affect the PE-induced reduction in KChIP2 mRNA level, whereas activation of PKC with phorbol ester (phorbol myristate [PMA]) causes a marked reduction in KChIP2 mRNA level. Pharmacological inhibition of MEKs or overexpression of a dominant-negative MEK1 increases the basal KChIP2 mRNA expression and blocks the PMA-induced decrease in auxiliary subunit mRNA level. In addition, a constitutively active MEK1 decreases the basal KChIP2 mRNA level, and PMA causes no further reduction in auxiliary subunit mRNA level in active MEK1-expressing cells. Furthermore, pharmacological inhibition of JNKs or overexpression of a dominant-negative JNK1 prevents the PE-induced, but not PMA-induced, reduction in KChIP2 mRNA expression. These results suggest that downregulation of KChIP2 expression significantly contributes to the hypertrophy-associated reduction in Ito density. They also indicate that the expression of KChIP2 mRNA is controlled by the 2 branches of mitogen-activated protein kinase pathways: JNKs play a predominant role in mediating the PE-induced reduction, whereas the MEK-ERK pathway influences the basal expression and mediates the PKC-mediated downregulation.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.