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- W2022142440 abstract "Significance Normal cardiac function requires coordinated contraction of working myocytes, which is initiated by a specific communication between Ca 2+ channels on the transverse (T)-tubule membrane and ryanodine receptors on the sarcoplasmic reticulum (SR) membrane. Junctophilin-2 (JP2) is a structural protein that induces docking of SR to T-tubules to form dyads and that indirectly stabilizes the T-tubule network in ventricular cardiomyocytes. JP2 is frequently down-regulated in heart failure, in parallel with a disruption of the T-tubule network and loss of normal excitation-contraction coupling. Here we show that overexpression of JP2 stabilizes the T-tubule network and attenuates heart failure after cardiac stress. These data suggest that future treatment of heart disease may include strategies to stabilize the architecture of T-tubules and cardiac dyads." @default.
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- W2022142440 date "2014-08-04" @default.
- W2022142440 modified "2023-10-17" @default.
- W2022142440 title "Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress" @default.
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- W2022142440 doi "https://doi.org/10.1073/pnas.1412729111" @default.
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