对心脏瑞诺丁受体FRET生物传感器的分子机制 病理性泄漏状态

Bengt Svensson1, Florentin R Nitu1, Robyn T Rebbeck1

  • 1Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.

概括

一种外源性 (DPc10) 和calmodulin (CaM) 调节心脏氨酸受体2 (RyR2) 通道活性. 了解它们的相互作用揭示了针对RyR2在心律失常的药物发现中的机制.

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