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Nature, ISSN 0028-0836, 07/2017, Volume 547, Issue 7662, pp. 227 - 231
The regenerative capacity of the adult mammalian heart is limited, because of the reduced ability of cardiomyocytes to progress through mitosis(1). Endogenous... 
PRESSURE-OVERLOAD | GENE | ADULT HEART REGENERATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | MOUSE MODEL | MUSCLE | DUCHENNE MUSCULAR-DYSTROPHY | MICE | Protein-Serine-Threonine Kinases - deficiency | Phosphorylation | Cell Proliferation | Glycoproteins - metabolism | Dystroglycans - metabolism | Male | Phosphoproteins - metabolism | Heart Failure - prevention & control | Multiprotein Complexes - metabolism | Dystrophin - deficiency | Mice, Inbred mdx | Cardiomyopathies | Glycoproteins - deficiency | Multiprotein Complexes - deficiency | Dystrophin - metabolism | Protein-Serine-Threonine Kinases - metabolism | Myocytes, Cardiac - cytology | Mice, Inbred C57BL | Organ Size | Heart Failure - genetics | Pressure | Multiprotein Complexes - chemistry | Animals | Dystrophin - genetics | Myocytes, Cardiac - metabolism | Protein Binding | Mice | Muscular Dystrophy, Duchenne - metabolism | Muscular Dystrophy, Duchenne - genetics | Adaptor Proteins, Signal Transducing - metabolism | Heart | Genes | Homeostasis | Genomes | Kinases | Muscular dystrophy | Cell growth | Actin | Duchenne's muscular dystrophy | Cell cycle | Extracellular matrix | Heart diseases | Dystrophin | Deoxyribonucleic acid--DNA | Heart failure | Dystroglycan | Glycoprotein | Cardiomyocytes | Studies | Yes-associated protein | Regeneration | Point mutation | Cytoskeleton | Dystrophy | Mutation | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 10/2017, Volume 550, Issue 7675, pp. 260 - 264
Mammalian organs vary widely in regenerative capacity. Poorly regenerative organs, such as the heart are particularly vulnerable to organ failure. Once... 
SURVIVAL | APOPTOSIS | MYOCARDIAL-INFARCTION | REGENERATION | TAMOXIFEN | MULTIDISCIPLINARY SCIENCES | INJURY | DYNAMICS | GENERATION | CARDIAC FIBROSIS | TRANSGENIC MICE | Genetic Therapy | Myocardial Infarction - genetics | Protein-Serine-Threonine Kinases - deficiency | Cell Proliferation | Humans | RNA, Messenger - metabolism | Heart Failure, Systolic - pathology | Myocardial Infarction - pathology | Cell Cycle Proteins - genetics | Protein-Serine-Threonine Kinases - metabolism | Quality Control | Heart Failure, Systolic - etiology | Myocytes, Cardiac - cytology | Heart Failure, Systolic - therapy | RNA, Messenger - genetics | Cell Cycle Proteins - metabolism | Protein-Serine-Threonine Kinases - genetics | Cell Cycle Proteins - deficiency | Signal Transduction - genetics | Mice, Knockout | Heart Failure, Systolic - metabolism | Myocardial Infarction - complications | Myocytes, Cardiac - pathology | Animals | Myocytes, Cardiac - metabolism | Mice | Ubiquitin-Protein Ligases - genetics | Heart failure | Complications and side effects | Infarction | Cellular signal transduction | Health aspects | Risk factors | Myocardial infarction | Heart | Purification | Heart attacks | Genes | Organs | Viruses | Cardiomyocytes | mRNA | Heart function | Kinases | Gene expression | Mitochondria | Clonal deletion | Ribonucleic acids | Quality control | Fibrosis | Myocardium | Fibroblasts | Gene therapy | Heart diseases | Growth factors | Index Medicus
Journal Article
Nature, ISSN 0028-0836, 05/2016, Volume 534, Issue 7605, pp. 119 - 123
Myocardial infarction results in compromised myocardial function and heart failure owing to insufficient cardiomyocyte self-renewal(1). Unlike many... 
RIEGER-SYNDROME | ELEMENTS | OXIDATIVE STRESS | GENE | REGENERATION | MULTIDISCIPLINARY SCIENCES | CARDIOMYOCYTE PROLIFERATION | GROWTH | ENHANCERS | GENOME | FAMILY | Heart Injuries - pathology | Myocardial Infarction - genetics | Protein-Serine-Threonine Kinases - deficiency | Electron Transport - drug effects | Reactive Oxygen Species - metabolism | Antioxidants - metabolism | Electron Transport - genetics | Heart Injuries - metabolism | Homeodomain Proteins - metabolism | Transcription Factors - deficiency | Male | Phosphoproteins - metabolism | Regeneration - genetics | Myocardial Infarction - pathology | Myocardium - metabolism | Female | Wound Healing - genetics | Wound Healing - drug effects | Disease Models, Animal | Animals, Newborn | Heart Injuries - genetics | Free Radical Scavengers - metabolism | Antioxidants - pharmacology | Myocardial Infarction - metabolism | Transcription Factors - genetics | Regeneration - physiology | Homeodomain Proteins - genetics | Transcription Factors - metabolism | Myocytes, Cardiac - pathology | Regeneration - drug effects | Animals | Myocytes, Cardiac - drug effects | NF-E2-Related Factor 2 - metabolism | Myocytes, Cardiac - metabolism | Heart Ventricles - metabolism | Mice | Wound Healing - physiology | Adaptor Proteins, Signal Transducing - metabolism | Heart Ventricles - drug effects | Heart | Physiological aspects | Genetic aspects | Regeneration (Biology) | Homeobox genes | Homeotic genes | Antioxidants | Transcription factors | Genetic regulation | Health aspects | Heart attack | Proteins | Heart attacks | Genes | DNA methylation | Cardiomyocytes | Kinases | Deoxyribonucleic acid--DNA | Index Medicus
Journal Article
Development, ISSN 0950-1991, 05/2004, Volume 131, Issue 9, pp. 2195 - 2204
Journal Article
Scientific Reports, ISSN 2045-2322, 12/2018, Volume 8, Issue 1, pp. 9955 - 11
Vasodilator-stimulated phosphoprotein (VASP) is a member of actin regulatory proteins implicated in platelet adhesion. In addition, phosphorylation of VASP is... 
SMOOTH-MUSCLE | FOCAL ADHESION | INHIBITION | TICAGRELOR | PHOSPHORYLATION | THROMBOSIS | MULTIDISCIPLINARY SCIENCES | ACUTE CORONARY SYNDROMES | RECEPTORS | INTACT HUMAN PLATELETS | ADP | Thrombocytopenia | CRISPR | Adenosine | Phosphorylation | Ferric chloride | Platelet aggregation | Thrombosis | Vasodilator-stimulated phosphoprotein | Actin | Collagen | Genotypes | P-selectin | Regulatory proteins
Journal Article
Nature Cell Biology, ISSN 1465-7392, 11/2013, Volume 15, Issue 11, pp. 1282 - 1293
Journal Article
by Howard, James F and Utsugisawa, Kimiaki and Benatar, Michael and Murai, Hiroyuki and Barohn, Richard J and Illa, Isabel and Jacob, Saiju and Vissing, John and Burns, Ted M and Kissel, John T and Muppidi, Srikanth and Nowak, Richard J and O'Brien, Fanny and Wang, Jing-Jing and Mantegazza, Renato and Mazia, Claudio Gabriel and Wilken, Miguel and Ortea, Carolina and Saba, Juliet and Rugiero, Marcelo and Bettini, Mariela and Vidal, Gonzalo and Vidal, Nuria and Garcia, Rebekah and Garcia, Sonia and Garcia, Alejandra Dalila and Lamont, Phillipa and Leong, Wai-Kuen and Boterhoven, Heidi and Fyfe, Beverly and Roberts, Leslie and Jasinarachchi, Mahi and Willlems, Natasha and Wanschitz, Julia and Löscher, Wolfgang and De Bleecker, Jan and Van den Abeele, Guy and de Koning, Kathy and De Mey, Katrien and Mercelis, Rudy and Wagemaekers, Linda and Mahieu, Delphine and Van Damme, Philip and Smetcoren, Charlotte and Stevens, Olivier and Verjans, Sarah and D'Hondt, Ann and Tilkin, Petra and Alves de Siqueira Carvalho, Alzira and Hasan, Rosa and Dias Brockhausen, Igor and Feder, David and Ambrosio, Daniel and Melo, Ana Paula and Rocha, Rosana and Rosa, Bruno and Veiga, Thabata and Augusto da Silva, Luiz and Gonçalves Geraldo, Jordana and da Penha Morita Ananias, Maria and Nogueira Coelho, Erica and Paiva, Gabriel and Pozo, Marina and Prando, Natalia and Dada Martineli Torres, Debora and Fernanda Butinhao, Cristiani and Coelho, Erica and Renata Cubas Volpe, Luciana and Duran, Gustavo and Gomes da Silva, Tamires Cristina and Otavio Maia Gonçalves, Luiz and Pazetto, Lucas Eduardo and Souza Duca, Luciana and Suriane Fialho, Tomás Augusto and Gheller Friedrich, Maurício André and Guerreiro, Alexandre and Mohr, Henrique and Pereira Martins, Maurer and da Cruz Pacheco, Daiane and Macagnan, Ana Paula and de Cassia Santos, Aline and Bulle Oliveira, Acary Souza and Amaral de Andrade, Ana Carolina and Annes, Marcelo and Cavalcante Lino, Valeria and Pinto, Wladimir and Miranda, Carolina and Carrara, Fernanda and Souza, Iandra and Genge, Angela and Massie, Rami and Campbell, Natasha and Bril, Vera and Katzberg, Hans and Soltani, Mehran and Ng, Eduardo and Siddiqi, Zaeem and Phan, Celile and Blackmore, Derrick and Vohanka, Stanislav and ... and REGAIN Study Grp and REGAIN Study Group
The Lancet Neurology, ISSN 1474-4422, 12/2017, Volume 16, Issue 12, pp. 976 - 986
Journal Article
Nature, ISSN 0028-0836, 07/2017, Volume 547, Issue 7662, p. 227
Journal Article