S
Saskia Schlossarek
Researcher at University of Hamburg
Publications - 51
Citations - 2511
Saskia Schlossarek is an academic researcher from University of Hamburg. The author has contributed to research in topics: Hypertrophic cardiomyopathy & Cardiomyopathy. The author has an hindex of 24, co-authored 45 publications receiving 2145 citations. Previous affiliations of Saskia Schlossarek include Cincinnati Children's Hospital Medical Center & VU University Medical Center.
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Journal ArticleDOI
Cardiac Myosin-Binding Protein C Mutations and Hypertrophic Cardiomyopathy : Haploinsufficiency, Deranged Phosphorylation, and Cardiomyocyte Dysfunction
Sabine J. van Dijk,Dennis Dooijes,Cris dos Remedios,Michelle Michels,Jos M. J. Lamers,Saul Winegrad,Saskia Schlossarek,Lucie Carrier,Folkert J. Ten Cate,Ger J.M. Stienen,Jolanda van der Velden +10 more
TL;DR: The frameshift MYBPC3 mutations cause haploinsufficiency, deranged phosphorylation of contractile proteins, and reduced maximal force-generating capacity of cardiomyocytes, and the enhanced Ca2+ sensitivity in MYB PC3mut is due to hypophosphorylation in troponin I secondary to mutation-induced dysfunction.
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Decreased phosphorylation levels of cardiac myosin-binding protein-C in human and experimental heart failure
Ali El-Armouche,Lutz Pohlmann,Saskia Schlossarek,Jutta Starbatty,Yung-Hsin Yeh,Stanley Nattel,Dobromir Dobrev,Thomas Eschenhagen,Lucie Carrier,Lucie Carrier +9 more
TL;DR: Cardiac myosin-binding protein-C phosphorylation levels are markedly decreased in human and experimental heart failure, suggesting that the compromised contractile function of the failing heart might be in part attributable to reduced cMyBP-C phosphate levels.
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The ubiquitin-proteasome system in cardiac dysfunction.
TL;DR: This review mainly focuses on the ubiquitin-proteasome system and its various components in healthy and diseased heart, but also summarizes recent data suggesting parallel activation of the UPS and autophagy in cardiac disease.
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Nonsense-Mediated mRNA Decay and Ubiquitin–Proteasome System Regulate Cardiac Myosin-Binding Protein C Mutant Levels in Cardiomyopathic Mice
Nicolas Vignier,Saskia Schlossarek,Bodvael Fraysse,Giulia Mearini,Elisabeth Krämer,Hervé Pointu,Nathalie Mougenot,Josiane Guiard,Rudolph Reimer,Heinrich Hohenberg,Ketty Schwartz,Muriel Vernet,Thomas Eschenhagen,Lucie Carrier +13 more
TL;DR: An unanticipated complexity of the expression of a single point mutation in the whole animal is revealed and the involvement of both nonsense-mediated mRNA decay and the ubiquitin–proteasome system in lowering the level of mutant proteins is revealed.
Journal ArticleDOI
Cardiac Myosin-Binding Protein C Is Required for Complete Relaxation in Intact Myocytes
Lutz Pohlmann,Irena Kröger,Nicolas Vignier,Saskia Schlossarek,Elisabeth Krämer,Catherine Coirault,Karim R. Sultan,Ali El-Armouche,Saul Winegrad,Thomas Eschenhagen,Lucie Carrier +10 more
TL;DR: It is shown that cMyBP-C functions as a restraint on myosin-actin interaction at low Ca2+ and short SL to allow complete relaxation during diastole, and this results in a defect in diastolic relaxation and a smaller dynamic range of cell shortening.