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Cardiac-specific, inducible ClC-3 gene deletion eliminates native volume-sensitive chloride channels and produces myocardial hypertrophy in adult mice.
TLDR
Results indicate that ClC-3 is a key component of native VSOACs in mammalian heart and plays a significant cardioprotective role against cardiac hypertrophy and failure. Expand
Myotendinous junction defects and reduced force transmission in mice that lack alpha7 integrin and utrophin.
TLDR
The alpha7/utr(-/-) mouse demonstrates the critical roles of alpha7 integrin and utrophin in maintaining myotendinous junction structure and enabling force transmission during muscle contraction, and indicates that the alpha7beta1 integrin, dystrophin, and utphin complexes act in a concerted manner to maintain the structural and functional integrity of skeletal muscle. Expand
CARDIAC‐SPECIFIC OVEREXPRESSION OF THE HUMAN SHORT CLC‐3 CHLORIDE CHANNEL ISOFORM IN MICE
TLDR
Enhanced VSOAC currents and acceleration of the time‐course of RVD in atrial myocytes of OE mice is strong evidence supporting an essential role of sClC‐3 in native VSOac function in mouse atrialMyocytes. Expand