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对Cavβ2的化定位克服了L型通道密度的失调并恢复了心脏功能

Francesca Rusconi1, Paola Ceriotti1, Michele Miragoli

  • 1From Humanitas Clinical and Research Center, Rozzano, Milan, Italy (F.R., P. Ceriotti, M.M., P. Carullo, N.S., E.D.P., P.K., M.-L.B., G.C., D.C.); Institute of Genetic and Biomedical Research UOS Milan National Research Council, Milan, Italy (F.R., P. Carullo, N.S., E.D.P., M.-L.B., D.C.); Department of Biotechnologies and Biosciences, University of Milan-Bicocca, Milan, Italy (M.R., A.Z.); Departments of Life Sciences (S.R.) and Clinical and Experimental Medicine (M.M.), University of Parma, Parma, Italy; University Hospital of Verona, Division of Cardiac Surgery, Verona, Italy (M.T., G.F.); Department of Sciences, University of Roma Tre, Rome, Italy (S.C., F.P.); University of Montpellier, CNRS UMR 5203, INSERM, Department of Neuroscience, Institute for Functional Genomics, LabEx Ion Channel Science and Therapeutics, Montpellier, France (M.C., J.C.); and National Institute of Nuclear Physics, Rome Tre Section, Rome, Italy (F.P.).

Circulation
|August 4, 2016
PubMed
概括

这项研究揭示了Akt依赖的Cavβ2酸化如何调节心脏中的L型通道 (LTCC). 一种针对Cavβ2的新型可以在糖尿病小鼠模型中恢复心脏功能.

关键词:
没有通道,L型心血管疾病糖尿病心肌病药物治疗类蛋白质运输

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