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1
Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression
Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression
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Quaking Inhibits Doxorubicin-Mediated Cardiotoxicity Through Regulation of Cardiac Circular RNA Expression

Circulation research, 2018-01, Vol.122 (2), p.246-254 [Peer Reviewed Journal]

2018 American Heart Association, Inc. ;2017 The Authors. ;Copyright Lippincott Williams & Wilkins Ovid Technologies Jan 19, 2018 ;2017 The Authors. 2017 ;ISSN: 0009-7330 ;EISSN: 1524-4571 ;DOI: 10.1161/CIRCRESAHA.117.311335 ;PMID: 29133306

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2
Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro
Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro
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Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro

Nature communications, 2019-01, Vol.10 (1), p.117-117, Article 117 [Peer Reviewed Journal]

This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-018-08003-1 ;PMID: 30631059

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3
SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes
SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes
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SARS-CoV-2 infects and induces cytotoxic effects in human cardiomyocytes

Cardiovascular Research, 2020-12, Vol.116 (14), p.2207-2215 [Peer Reviewed Journal]

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com. 2020 ;Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions, please email: journals.permissions@oup.com. ;2020. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at https://academic.oup.com/journals/pages/coronavirus . ;Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020. For permissions please email: journals.permissions@oup.com. 2020 ;ISSN: 0008-6363 ;EISSN: 1755-3245 ;DOI: 10.1093/cvr/cvaa267 ;PMID: 32966582

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4
Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants
Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants
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Increased susceptibility of human endothelial cells to infections by SARS-CoV-2 variants

Basic research in cardiology, 2021-07, Vol.116 (1), p.42-42, Article 42 [Peer Reviewed Journal]

The Author(s) 2021 ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;ISSN: 0300-8428 ;EISSN: 1435-1803 ;DOI: 10.1007/s00395-021-00882-8 ;PMID: 34224022

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5
Diabetes Mellitus–Induced Microvascular Destabilization in the Myocardium
Diabetes Mellitus–Induced Microvascular Destabilization in the Myocardium
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Diabetes Mellitus–Induced Microvascular Destabilization in the Myocardium

Journal of the American College of Cardiology, 2017-01, Vol.69 (2), p.131-143 [Peer Reviewed Journal]

American College of Cardiology Foundation ;2017 American College of Cardiology Foundation ;Copyright © 2017 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. ;COPYRIGHT 2017 Elsevier B.V. ;Copyright Elsevier Limited Jan 17, 2017 ;ISSN: 0735-1097 ;EISSN: 1558-3597 ;DOI: 10.1016/j.jacc.2016.10.058 ;PMID: 28081822

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6
MicroRNA-365 regulates human cardiac action potential duration
MicroRNA-365 regulates human cardiac action potential duration
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MicroRNA-365 regulates human cardiac action potential duration

Nature communications, 2022-01, Vol.13 (1), p.220-220, Article 220 [Peer Reviewed Journal]

2022. The Author(s). ;The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2022 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-021-27856-7 ;PMID: 35017523

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7
Human Induced Pluripotent Stem-Cell-Derived Cardiomyocytes as Models for Genetic Cardiomyopathies
Human Induced Pluripotent Stem-Cell-Derived Cardiomyocytes as Models for Genetic Cardiomyopathies
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Human Induced Pluripotent Stem-Cell-Derived Cardiomyocytes as Models for Genetic Cardiomyopathies

International journal of molecular sciences, 2019-09, Vol.20 (18), p.4381 [Peer Reviewed Journal]

2019. This work is licensed under https://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2019 by the authors. 2019 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms20184381 ;PMID: 31489928

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8
Cardiac desmosomal adhesion relies on ideal-, slip- and catch bonds
Cardiac desmosomal adhesion relies on ideal-, slip- and catch bonds
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Cardiac desmosomal adhesion relies on ideal-, slip- and catch bonds

Scientific reports, 2024-01, Vol.14 (1), p.2555-2555, Article 2555 [Peer Reviewed Journal]

2024. The Author(s). ;The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2024 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-024-52725-w ;PMID: 38297017

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9
Novel Desmin Mutation p.Glu401Asp Impairs Filament Formation, Disrupts Cell Membrane Integrity, and Causes Severe Arrhythmogenic Left Ventricular Cardiomyopathy/Dysplasia
Novel Desmin Mutation p.Glu401Asp Impairs Filament Formation, Disrupts Cell Membrane Integrity, and Causes Severe Arrhythmogenic Left Ventricular Cardiomyopathy/Dysplasia
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Novel Desmin Mutation p.Glu401Asp Impairs Filament Formation, Disrupts Cell Membrane Integrity, and Causes Severe Arrhythmogenic Left Ventricular Cardiomyopathy/Dysplasia

Circulation (New York, N.Y.), 2018-04, Vol.137 (15), p.1595-1610 [Peer Reviewed Journal]

2018 by the American College of Cardiology Foundation and the American Heart Association, Inc. ;2017 American Heart Association, Inc. ;ISSN: 0009-7322 ;EISSN: 1524-4539 ;DOI: 10.1161/CIRCULATIONAHA.117.028719 ;PMID: 29212896

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10
The N-Terminal Part of the 1A Domain of Desmin Is a Hot Spot Region for Putative Pathogenic DES Mutations Affecting Filament Assembly
The N-Terminal Part of the 1A Domain of Desmin Is a Hot Spot Region for Putative Pathogenic DES Mutations Affecting Filament Assembly
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The N-Terminal Part of the 1A Domain of Desmin Is a Hot Spot Region for Putative Pathogenic DES Mutations Affecting Filament Assembly

Cells (Basel, Switzerland), 2022-12, Vol.11 (23), p.3906 [Peer Reviewed Journal]

2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2022 by the authors. 2022 ;EISSN: 2073-4409 ;DOI: 10.3390/cells11233906 ;PMID: 36497166

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11
Targeting myeloid cell coagulation signaling blocks MAP kinase/TGF-β1-driven fibrotic remodeling in ischemic heart failure
Targeting myeloid cell coagulation signaling blocks MAP kinase/TGF-β1-driven fibrotic remodeling in ischemic heart failure
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Targeting myeloid cell coagulation signaling blocks MAP kinase/TGF-β1-driven fibrotic remodeling in ischemic heart failure

The Journal of clinical investigation, 2023-02, Vol.133 (4), p.1-21 [Peer Reviewed Journal]

Copyright American Society for Clinical Investigation Feb 2023 ;2023 Garlapati et al. 2023 Garlapati et al. ;ISSN: 1558-8238 ;ISSN: 0021-9738 ;EISSN: 1558-8238 ;DOI: 10.1172/JCI156436 ;PMID: 36548062

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12
Neprilysins regulate muscle contraction and heart function via cleavage of SERCA-inhibitory micropeptides
Neprilysins regulate muscle contraction and heart function via cleavage of SERCA-inhibitory micropeptides
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Neprilysins regulate muscle contraction and heart function via cleavage of SERCA-inhibitory micropeptides

Nature communications, 2022-07, Vol.13 (1), p.4420-4420, Article 4420 [Peer Reviewed Journal]

The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2022 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-022-31974-1 ;PMID: 35906206

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13
Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure
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Detrimental proarrhythmogenic interaction of Ca2+/calmodulin-dependent protein kinase II and NaV1.8 in heart failure

Nature communications, 2021-11, Vol.12 (1), p.1-13, Article 6586 [Peer Reviewed Journal]

The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-021-26690-1 ;PMID: 34782600

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14
Screening for mutations in human cardiomyopathy- is RBM24 a new but rare disease gene?
Screening for mutations in human cardiomyopathy- is RBM24 a new but rare disease gene?
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Screening for mutations in human cardiomyopathy- is RBM24 a new but rare disease gene?

Protein & cell, 2019-06, Vol.10 (6), p.393-394 [Peer Reviewed Journal]

Copyright reserved, 2018, The Author(s) ;The Author(s) 2018 ;Protein & Cell is a copyright of Springer, (2018). All Rights Reserved. © 2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;ISSN: 1674-800X ;EISSN: 1674-8018 ;DOI: 10.1007/s13238-018-0590-z ;PMID: 30421357

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15
The disease-specific phenotype in cardiomyocytes derived from induced pluripotent stem cells of two long QT syndrome type 3 patients
The disease-specific phenotype in cardiomyocytes derived from induced pluripotent stem cells of two long QT syndrome type 3 patients
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The disease-specific phenotype in cardiomyocytes derived from induced pluripotent stem cells of two long QT syndrome type 3 patients

PloS one, 2013-12, Vol.8 (12), p.e83005-e83005 [Peer Reviewed Journal]

COPYRIGHT 2013 Public Library of Science ;COPYRIGHT 2013 Public Library of Science ;2013 Fatima et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2013 Fatima et al 2013 Fatima et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0083005 ;PMID: 24349418

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16
Special Issue "Cardiovascular Genetics"
Special Issue "Cardiovascular Genetics"
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Special Issue "Cardiovascular Genetics"

Genes, 2021-03, Vol.12 (4), p.479 [Peer Reviewed Journal]

2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2021 by the authors. 2021 ;ISSN: 2073-4425 ;EISSN: 2073-4425 ;DOI: 10.3390/genes12040479 ;PMID: 33810227

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17
Restrictive Cardiomyopathy is Caused by a Novel Homozygous Desmin ( DES ) Mutation p.Y122H Leading to a Severe Filament Assembly Defect
Restrictive Cardiomyopathy is Caused by a Novel Homozygous Desmin ( DES ) Mutation p.Y122H Leading to a Severe Filament Assembly Defect
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Restrictive Cardiomyopathy is Caused by a Novel Homozygous Desmin ( DES ) Mutation p.Y122H Leading to a Severe Filament Assembly Defect

Genes, 2019-11, Vol.10 (11), p.918 [Peer Reviewed Journal]

2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2019 by the authors. 2019 ;ISSN: 2073-4425 ;EISSN: 2073-4425 ;DOI: 10.3390/genes10110918 ;PMID: 31718026

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18
Publisher Correction: Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro
Publisher Correction: Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro
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Publisher Correction: Long-term functional and structural preservation of precision-cut human myocardium under continuous electromechanical stimulation in vitro

Nature communications, 2019-01, Vol.10 (1), p.532-532, Article 532 [Peer Reviewed Journal]

This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-019-08510-9 ;PMID: 30692546

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19
High proportion of genetic cases in patients with advanced cardiomyopathy including a novel homozygous Plakophilin 2-gene mutation
High proportion of genetic cases in patients with advanced cardiomyopathy including a novel homozygous Plakophilin 2-gene mutation
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High proportion of genetic cases in patients with advanced cardiomyopathy including a novel homozygous Plakophilin 2-gene mutation

PloS one, 2017-12, Vol.12 (12), p.e0189489-e0189489 [Peer Reviewed Journal]

COPYRIGHT 2017 Public Library of Science ;COPYRIGHT 2017 Public Library of Science ;2017 Klauke et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2017 Klauke et al 2017 Klauke et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0189489 ;PMID: 29253866

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20
Hemi- and Homozygous Loss-of-Function Mutations in DSG2 (Desmoglein-2) Cause Recessive Arrhythmogenic Cardiomyopathy with an Early Onset
Hemi- and Homozygous Loss-of-Function Mutations in DSG2 (Desmoglein-2) Cause Recessive Arrhythmogenic Cardiomyopathy with an Early Onset
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Hemi- and Homozygous Loss-of-Function Mutations in DSG2 (Desmoglein-2) Cause Recessive Arrhythmogenic Cardiomyopathy with an Early Onset

International journal of molecular sciences, 2021-04, Vol.22 (7), p.3786 [Peer Reviewed Journal]

2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2021 by the authors. 2021 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms22073786 ;PMID: 33917638

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