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1. Full Text L’espace d’une pensée. Lucie Roy, Le pouvoir de l’oubliée : la perception au cinéma, Paris, L’Harmattan, coll. « Esthétiques », 2015, 235 p
by Carrier-Lafleur, Thomas
Cinémas: Revue d'études cinématographiques, ISSN 1181-6945, 2016, Volume 27, Issue 1, p. 157
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2. Full Text MYBPC3 Gene Therapy for Neonatal Sarcomeric Cardiomyopathies
by Carrier, Lucie
Biophysical Journal, ISSN 0006-3495, 01/2015, Volume 108, Issue 2, pp. 34a - 34a
Infants (Newborn) | Gene therapy | Care and treatment
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3. Full Text Making Sense of Inhibiting Nonsense in Hypertrophic Cardiomyopathy
by Carrier, Lucie
Circulation, ISSN 0009-7322, 02/2019, Volume 139, Issue 6, pp. 812 - 814
myocytes, cardiac | proteasome inhibitors | Editorials | autophagy | cardiomyopathy, hypertrophic | regeneration | MYBPC3 | CARDIAC & CARDIOVASCULAR SYSTEMS | SURVEILLANCE | PERIPHERAL VASCULAR DISEASE | MESSENGER-RNA DECAY | MUTATIONS | EXPRESSION
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4. Full Text Cardiomyopathy phenotypes in human-induced pluripotent stem cell-derived cardiomyocytes—a systematic review
by Eschenhagen, Thomas and Carrier, Lucie
Pflügers Archiv - European Journal of Physiology, ISSN 0031-6768, 5/2019, Volume 471, Issue 5, pp. 755 - 768
Human-induced pluripotent stem cells (hiPSC) can be differentiated to cardiomyocytes at high efficiency and are increasingly used to study cardiac disease in a... 
Quantitative phenotypes | Neurosciences | Receptors | Biomedicine | Human Physiology | hiPSC | Cardiomyopathy | Disease modelling | Molecular Medicine | Cell Biology | Medical research | Heart cells | T cells | Muscle proteins | Gene expression | Phenotype | Analysis | Stem cells | Myosin | Medicine, Experimental | Genetic aspects | Heart diseases | Phenotypes | Transcription factors | Cardiomyocytes | NF-AT protein | Coronary artery disease | Dilated cardiomyopathy | Cell size | Localization | Pluripotency | Invited Review
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5. Full Text Ubiquitin-proteasome system and hereditary cardiomyopathies
by Schlossarek, Saskia and Frey, Norbert and Carrier, Lucie
Journal of Molecular and Cellular Cardiology, ISSN 0022-2828, 2013, Volume 71, pp. 25 - 31
Abstract Adequate protein turnover is essential for cardiac homeostasis. Different protein quality controls are involved in the maintenance of protein... 
Cardiovascular | Dilated cardiomyopathy | Hypertrophic cardiomyopathy | Ubiquitin-proteasome system | Heart - physiopathology | Sarcomeres - metabolism | Humans | Ubiquitin - metabolism | Ubiquitin-Protein Ligases - metabolism | Myocardium - pathology | Autophagy - physiology | Cardiomyopathies - genetics | Cardiomyopathies - physiopathology | Animals | Cardiomyopathies - metabolism | Myocardium - metabolism | Proteasome Endopeptidase Complex - metabolism | Ubiquitin | Index Medicus
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6. Full Text Gene therapy strategies in the treatment of hypertrophic cardiomyopathy
by Prondzynski, Maksymilian and Mearini, Giulia and Carrier, Lucie
Pflügers Archiv - European Journal of Physiology, ISSN 0031-6768, 5/2019, Volume 471, Issue 5, pp. 807 - 815
Hypertrophic cardiomyopathy (HCM) is an inherited myocardial disease with an estimated prevalence of 1:200 caused by mutations in sarcomeric proteins. It is... 
MYBPC3 | Gene replacement | Neurosciences | Human Physiology | CRISPR/Cas9 | Cell Biology | trans -splicing | Receptors | Biomedicine | Exon skipping | Hypertrophic cardiomyopathy | Molecular Medicine | Gene therapy | trans-splicing | CRISPR | BINDING-PROTEIN-C | DIAGNOSIS | PHYSIOLOGY | CRISPR/CAS9 | SUDDEN-DEATH | PHENOTYPE | DELIVERY | CALCIUM UP-REGULATION | DISEASE | MUTATION | Cas9 | Proteins | Medical research | Anopheles | Care and treatment | Cardiomyopathy, Hypertrophic | RNA | Analysis | Genes | Genomics | Stem cells | Medicine, Experimental | Cell culture | Splicing | Cardiomyopathy | RNA-mediated interference | Genomes | Ribonucleic acid--RNA | Gene silencing | Fibrosis | Mutation | Ventricle | Pluripotency | Hypertrophy
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7. Full Text Too much of a good thing is bad: Proteasome inhibition induces stressed hearts to fail
by Carrier, Lucie
Cardiovascular Research, ISSN 0008-6363, 12/2010, Volume 88, Issue 3, pp. 389 - 390
SYSTEM | PRESSURE-OVERLOAD | CARDIAC & CARDIOVASCULAR SYSTEMS | VENTRICULAR HYPERTROPHY | BORTEZOMIB | CARDIAC PROTEASOME | Heart Failure - physiopathology | Boronic Acids - adverse effects | NFATC Transcription Factors - physiology | Dose-Response Relationship, Drug | Protease Inhibitors - pharmacology | Proteasome Endopeptidase Complex - drug effects | Protease Inhibitors - adverse effects | Models, Animal | Heart Failure - etiology | Stress, Physiological - physiology | Bortezomib | Hypertrophy, Left Ventricular - prevention & control | Adaptation, Physiological - physiology | Proteasome Endopeptidase Complex - physiology | Ubiquitin - physiology | Calcineurin - physiology | Animals | Myocytes, Cardiac - physiology | Pyrazines - adverse effects | Signal Transduction - physiology | Mice | Hypertrophy, Left Ventricular - physiopathology | Proteasome Inhibitors | Pyrazines - pharmacology | Boronic Acids - pharmacology | Index Medicus
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8. Full Text How do MYBPC3 mutations cause hypertrophic cardiomyopathy?
by Marston, Steven and Copeland, O’Neal and Gehmlich, Katja and Schlossarek, Saskia and Carrrier, Lucie
Journal of Muscle Research and Cell Motility, ISSN 0142-4319, 5/2012, Volume 33, Issue 1, pp. 75 - 80
It is well established that MYBPC3 mutations are the most common cause of hypertrophic cardiomyopathy, accounting for about half of identified mutations.... 
Life Sciences | MYBPC3 | Ca 2+ -regulation | Nonsense mediated RNA decay | Proteomics | Hypertrophic cardiomyopathy | Ubiquitin-proteasome system | Animal Anatomy / Morphology / Histology | MyBP-C | Biomedicine general | Cell Biology | Haploinsufficiency | regulation | BINDING-PROTEIN-C | PHOSPHORYLATION | SPLICE DONOR SITE | CONTRACTILE PROTEINS | CELL BIOLOGY | HUMAN HEART-MUSCLE | GENE | Ca2+-regulation | MICE | MESSENGER-RNA DECAY | Cardiomyopathy, Hypertrophic - genetics | Frameshift Mutation | Calcium - metabolism | Exons | Cardiomyopathy, Hypertrophic - metabolism | Humans | RNA, Messenger - genetics | Peptide Chain Termination, Translational | Myocardium - pathology | RNA, Messenger - metabolism | Nonsense Mediated mRNA Decay | Carrier Proteins - genetics | RNA Splicing | Animals | Carrier Proteins - metabolism | Myocardium - metabolism | Codon, Nonsense - metabolism | Codon, Nonsense - genetics | Cardiomyopathy, Hypertrophic - pathology | Proteins | Cardiomyopathy, Hypertrophic | RNA | Peptides | Cardiomyopathy | Genetic aspects | Heart diseases
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9. Full Text The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy
by Ucar, Ahmet and Gupta, Shashi K and Fiedler, Jan and Erikci, Erdem and Kardasinski, Michal and Batkai, Sandor and Dangwal, Seema and Kumarswamy, Regalla and Bang, Claudia and Holzmann, Angelika and Remke, Janet and Caprio, Massimiliano and Jentzsch, Claudia and Engelhardt, Stefan and Geisendorf, Sabine and Glas, Carolina and Hofmann, Thomas G and Nessling, Michelle and Richter, Karsten and Schiffer, Mario and Carrier, Lucie and Napp, L. Christian and Bauersachs, Johann and Chowdhury, Kamal and Thum, Thomas
Nature Communications, ISSN 2041-1723, 2012, Volume 3, Issue 1, p. 1078
Pathological growth of cardiomyocytes (hypertrophy) is a major determinant for the development of heart failure, one of the leading medical causes of mortality... 
ATROPHY | MOUSE MAMMARY-GLAND | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | IN-VIVO | CONDUCTION | MICE | MICRORNAS | TARGETED DELETION | STRESS | EXPRESSION | Oligonucleotides - genetics | Cells, Cultured | Rats | Male | Mice, Transgenic | Reverse Transcriptase Polymerase Chain Reaction | Animals | Calcineurin - genetics | Myocytes, Cardiac - metabolism | Mice | MicroRNAs - genetics | Autophagy - genetics | Cardiomegaly - genetics
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10. Full Text Cardiac myosin-binding protein C (MYBPC3) in cardiac pathophysiology
by Carrier, Lucie and Mearini, Giulia and Stathopoulou, Konstantina and Cuello, Friederike
Gene, ISSN 0378-1119, 12/2015, Volume 573, Issue 2, pp. 188 - 197
More than 350 individual mutations have been identified in patients with inherited hypertrophic cardiomyopathy (HCM), thus representing 40–50% of all HCM... 
MYBPC3 | Cardiomyopathies | Gene therapy | Cardiac myosin-binding protein C | Hypertrophy postranslational modifications | SARCOMERIC CARDIOMYOPATHIES | FAMILIAL HYPERTROPHIC CARDIOMYOPATHY | UBIQUITIN-PROTEASOME SYSTEM | KINASE-A | SUDDEN-DEATH | SPLICE DONOR SITE | DIASTOLIC DYSFUNCTION | LEFT-VENTRICULAR NONCOMPACTION | GENETICS & HEREDITY | MESSENGER-RNA DECAY | CMYBP-C | Carrier Proteins - physiology | Cardiomyopathies - genetics | Founder Effect | Genetic Therapy | Animals | Humans | Protein Processing, Post-Translational | Mutation | Cardiomyopathies - therapy | Protein C | Gene mutations | Muscle proteins | Cardiac patients | Myosin | Protein binding | Index Medicus | gene therapy | hypertrophy postranlational modifications | cardiomyopathies | cardiac myosin-binding protein C
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11. Full Text Ectosomes: A new mechanism for non-exosomal secretion of Tau protein
by Dujardin, Simon and Bégard, Séverine and Caillierez, Raphaëlle and Lachaud, Cédrick and Delattre, Lucie and Carrier, Sébastien and Loyens, Anne and Galas, Marie-Christine and Bousset, Luc and Melki, Ronald and Aurégan, Gwennaëlle and Hantraye, Philippe and Brouillet, Emmanuel and Buée, Luc and Colin, Morvane
PLoS ONE, ISSN 1932-6203, 06/2014, Volume 9, Issue 6, p. e100760
Tau is a microtubule-associated protein that aggregates in neurodegenerative disorders known as tauopathies. Recently, studies have suggested that Tau may be... 
NEUROFIBRILLARY TANGLES | EXTRACELLULAR VESICLES | MEMBRANE-VESICLES | ALZHEIMERS-DISEASE | MULTIDISCIPLINARY SCIENCES | PAIRED HELICAL FILAMENTS | CEREBROSPINAL-FLUID | NEUROBLASTOMA-CELLS | PLASMA-MEMBRANE | PROGRESSIVE SUPRANUCLEAR PALSY | CELL-DERIVED MICROPARTICLES | Exosomes - metabolism | Rats, Wistar | Humans | Cells, Cultured | Rats | tau Proteins - metabolism | Neurons - cytology | Microscopy, Electron | Extracellular Fluid - metabolism | Animals | Embryo, Mammalian - cytology | Cell-Derived Microparticles - metabolism | Neurons - metabolism | Deregulation | Immunoglobulins | Phosphorylation | Neurodegenerative diseases | Secretion | Membrane vesicles | Biochemistry | Cell interactions | Proteins | Signal transduction | Signaling | Vesicles | Cellular communication | Tau protein | Neurodegeneration | Neural networks | Physiology | Alzheimers disease | Life Sciences | Cognitive Sciences | Neurons and Cognition | Psychology and behavior | Neurobiology
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12. Genetics of Hypertrophic and Dilated Cardiomyopathy
by Friedrich, FW and Carrier, L
CURRENT PHARMACEUTICAL BIOTECHNOLOGY, ISSN 1389-2010, 10/2012, Volume 13, Issue 13, pp. 2467 - 2476
Cardiomyopathies are categorized as extrinsic, being caused by external factors, such as hypertension, ischemia, inflammation, valvular dysfunction, or as... 
BINDING-PROTEIN-C | UBIQUITIN-PROTEASOME SYSTEM | ANKYRIN REPEAT PROTEIN | Cardiomyopathy | hypertrophy | DISEASE GENE | BIOCHEMISTRY & MOLECULAR BIOLOGY | dilatation | HEART-FAILURE | MUSCLE LIM PROTEIN | MYOSIN HEAVY-CHAIN | mutation | genetics | CARDIAC TROPONIN-T | DREIFUSS MUSCULAR-DYSTROPHY | PHARMACOLOGY & PHARMACY | ALPHA-TROPOMYOSIN | Cardiomyopathy, Dilated - genetics | Cardiomyopathy, Hypertrophic - genetics | Sarcoplasmic Reticulum - genetics | Genetic Association Studies | Sarcomeres - genetics | Humans | Cytoskeleton - genetics | Mutation
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13. Full Text I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model
by Friedrich, Felix W and Sotoud, Hannieh and Geertz, Birgit and Weber, Silvio and Flenner, Frederik and Reischmann, Silke and Eschenhagen, Thomas and Carrier, Lucie and El-Armouche, Ali
IJC Heart & Vasculature, ISSN 2352-9067, 09/2015, Volume 8, Issue C, pp. 87 - 94
Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy, diastolic dysfunction and increased interstitial fibrosis. Current... 
Hypertrophic cardiomyopathy | Beta-adrenergic signalling | Cardiomyopathy | Hypertrophy
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14. Full Text Mybpc3 gene therapy for neonatal cardiomyopathy enables long-term disease prevention in mice
by Mearini, Giulia and Stimpel, Doreen and Geertz, Birgit and Weinberger, Florian and Krämer, Elisabeth and Schlossarek, Saskia and Mourot-Filiatre, Julia and Stoehr, Andrea and Dutsch, Alexander and Wijnker, Paul J. M and Braren, Ingke and Katus, Hugo A and Müller, Oliver J and Voit, Thomas and Eschenhagen, Thomas and Carrier, Lucie
Nature Communications, ISSN 2041-1723, 2014, Volume 5, Issue 1, pp. 5515 - 5515
Homozygous or compound heterozygous frameshift mutations in MYBPC3 encoding cardiac myosin-binding protein C (cMyBP-C) cause neonatal hypertrophic... 
BINDING-PROTEIN-C | HYPERTROPHIC CARDIOMYOPATHY | MESSENGER-RNA | MULTIDISCIPLINARY SCIENCES | KNOCK-IN MICE | COMPOUND MUTATIONS | ENGINEERED HEART-TISSUE | DYSFUNCTION | EXPRESSION | FAILURE | DELIVERY | Carrier Proteins - genetics | Homozygote | Animals | Carrier Proteins - metabolism | Cardiomyopathy, Hypertrophic, Familial - therapy | Cardiomyopathy, Hypertrophic, Familial - genetics | Cardiomyopathy, Hypertrophic, Familial - metabolism | Mice | Dependovirus | RNA, Messenger - metabolism | Gene Knock-In Techniques | Genetic Therapy - methods | Index Medicus
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