Learn More
Fragile X Mental Retardation Syndrome is the most common form of hereditary mental retardation, and is caused by defects in the FMR1 gene. FMR1 is an RNA-binding protein and the syndrome results from lack of expression of FMR1 or expression of a mutant protein that is impaired in RNA binding. The specific function of FMR1 is not known. As a step towards(More)
Pressure overload-induced hypertrophy is a key step leading to heart failure. The Ca(2+)-induced Ca(2+) release (CICR) process that governs cardiac contractility is defective in hypertrophy/heart failure, but the molecular mechanisms remain elusive. To examine the intermolecular aspects of CICR during hypertrophy, we utilized loose-patch confocal imaging to(More)
The genetic lesion in the quakingviable (qk(v)) mutant mice is a deletion 5' to the qkI gene, resulting in severe hypomyelination. qkI produces several QKI protein isoforms via alternative splicing of the C-terminal coding exons. In the qk(v)/qk(v) brain, immunostaining of QKI proteins is diminished in an isoform-differential manner with undefined(More)
Early identification for heart failure (HF) may be useful for disease modifying treatment in order to reduce heart disease progression or even to reverse it. In our previous studies, we have revealed a group of heat shock proteins (HSPs) which might be related to neonatal rat cardiomyocyte hypertrophy by proteomic approach. Here, we confirm that HSPs,(More)
The many kinds of cell structures involved in cell-cell communication include tight junction, adherens junction and gap junction, but almost all are between adjacent cells. Recently, a general and dynamic membrane tether, termed tunneling nanotubes or membrane nanotubes (MNTs), was discovered to be involved in communication between distant cells. By(More)
AIM beta-adrenergic receptor (beta-AR) agonists are among the most potent factors regulating cardiac electrophysiological properties. Connexin 43 (Cx43), the predominant gap-junction protein in the heart, has an indispensable role in modulating cardiac electric activities by affecting gap-junction function. The present study investigates the effects of(More)
Recent studies have begun to reveal critical roles of microRNAs (miRNAs) in the pathogenesis of cardiac hypertrophy and dysfunction. In this study, we tested whether a transforming growth factor-β (TGF-β)-regulated miRNA played a pivotal role in the development of cardiac hypertrophy and heart failure (HF). We observed that miR-27b was upregulated in hearts(More)
Background microRNAs (miRNAs) are a class of small, non-coding endogenous RNAs that post-transcriptionally regulate some protein-coding genes. miRNAs play an important role in many cardiac pathophysiological processes, including myocardial infarction, cardiac hypertrophy, and heart failure. miR-499, specifically expressed in skeletal muscle and cardiac(More)
AIMS The contraction of a heart cell is controlled by Ca(2+)-induced Ca(2+) release between L-type Ca(2+) channels (LCCs) in the cell membrane/T-tubules (TTs) and ryanodine receptors (RyRs) in the junctional sarcoplasmic reticulum (SR). During heart failure, LCC-RyR signalling becomes defective. The purpose of the present study was to reveal the(More)
AIMS It has been reported that cardiac ankyrin repeat protein is associated with heart development and diseases. This study is aimed to investigate the role of CARP in heart hypertrophy in vivo. METHODS AND RESULTS We generated a cardiac-specific CARP-overexpressing transgenic mouse. Although such animals did not display any overt physiological(More)