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      Arrhythmogenic right ventricular cardiomyopathy mutations alter shear response without changes in cell-cell adhesion.

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          Abstract

          The majority of patients diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC) have mutations in genes encoding desmosomal proteins, raising the possibility that abnormal intercellular adhesion plays an important role in disease pathogenesis. We characterize cell mechanical properties and molecular responses to oscillatory shear stress in cardiac myocytes expressing mutant forms of the desmosomal proteins, plakoglobin and plakophilin, which are linked to ARVC in patients.

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          Author and article information

          Journal
          Cardiovasc. Res.
          Cardiovascular research
          Oxford University Press (OUP)
          1755-3245
          0008-6363
          Nov 01 2014
          : 104
          : 2
          Affiliations
          [1 ] Department of Biomedical Engineering, Columbia University, 351 Engineering Terrace, 500 W 120th Street, MC 8904, New York, NY 10027, USA.
          [2 ] Department of Pathology, Beth Israel Deaconess Medical Center, Boston, MA, USA Department of Pathology, Harvard Medical School, Boston, MA, USA.
          [3 ] Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA Department of Medicine, Harvard Medical School, Boston, MA, USA.
          [4 ] Department of Biomedical Engineering, Columbia University, 351 Engineering Terrace, 500 W 120th Street, MC 8904, New York, NY 10027, USA hayden.huang@columbia.edu.
          Article
          cvu212
          10.1093/cvr/cvu212
          4296114
          25253076

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