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- W1998982561 abstract "AimsCardiac L-type Ca2+-currents show distinct alterations in chronic heart failure, including increased single-channel activity and blunted adrenergic stimulation, but minor changes of whole-cell currents. Expression of L-type Ca2+-channel β2-subunits is enhanced in human failing hearts. In order to determine whether prolonged alteration of Ca2+-channel gating by β2-subunits contributes to heart failure pathogenesis, we generated and characterized transgenic mice with cardiac overexpression of a β2a-subunit or the pore Cav1.2 or both, respectively." @default.
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- W1998982561 date "2009-07-20" @default.
- W1998982561 modified "2023-10-17" @default.
- W1998982561 title "Transgenic simulation of human heart failure-like L-type Ca2+-channels: implications for fibrosis and heart rate in mice" @default.
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- W1998982561 doi "https://doi.org/10.1093/cvr/cvp251" @default.
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