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Fig. 1 | BMC Cardiovascular Disorders

Fig. 1

From: HiPSC-derived cardiomyocyte to model Brugada syndrome: both asymptomatic and symptomatic mutation carriers reveal increased arrhythmogenicity

Fig. 1

Clinical background of asymptomatic and symptomatic individuals and generation and characterization of hiPSC-lines. (A) The pedigree of the family of asymptomatic (Brugada syndrome) and symptomatic brothers. (B) ECG from symptomatic individuals before (above) and 10 min after receiving flecainide (below). (C) Schematic representation of SCN5A channel protein. Mutation R1913C is located in the C-terminal of the protein. (D) Immunocytochemical stainings and expression of pluripotency markers. Scale bars 100 μm. (E) RT-PCR confirmed that none of the exogenous genes are expressed in iPSC lines. Images are cropped and merged, and full images available in additional file 1: Fig S3A (F) pluripotency markers are turned on. Images are cropped and merged, and full images available in additional file 1: Fig S3B-C and (G) EBs express markers from all the three embryonic germ layers. Images are cropped and merged, and full images available in additional file 1: Fig S3D. GAPDH serves as a housekeeping gene in all RT-PRC figures

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BMC Cardiovascular Disorders

ISSN: 1471-2261

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