Výsledky vyhledávání - "Silke Reischmann-Düsener"

Akademický článek

S100A4 as a Target of the E3-Ligase Asb2β and Its Effect on Engineered Heart Tissue

Autor: Simon Braumann, Tilo Thottakara, Sabrina Stücker, Silke Reischmann-Düsener, Elisabeth Krämer, Julia Groß, Marc N. Hirt, Shirin Doroudgar, Lucie Carrier, Felix W. Friedrich

Publikováno v: Frontiers in Physiology, Vol 9 (2018)

Background: S100A4 has recently emerged as an important player in cardiac disease, affecting phenotype development in animal models of myocardial infarction and pathological cardiac hypertrophy, albeit it is unclear whether S100A4 exerts a detrimenta

Externí odkaz: https://doaj.org/article/6c7a86c5281f4704851a5030e728a51d

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A high-throughput screening identifies ZNF418 as a novel regulator of the ubiquitin-proteasome system and autophagy-lysosomal pathway

Autor: Hanna Osinska, Ellen Orthey, Jeffery D. Molkentin, Saskia Schlossarek, Jeffrey Robbins, Erda Alizoti, Sonia R. Singh, James Gulick, W. Clark Bacon, Moritz Meyer-Jens, Lucie Carrier, Gregory Davis, Silke Reischmann-Düsener, Patrick M. McLendon

Publikováno v: Autophagy
article-version (VoR) Version of Record

The ubiquitin-proteasome system (UPS) and autophagy-lysosomal pathway (ALP) are two major protein degradation pathways in eukaryotic cells. Initially considered as two independent pathways, there is emerging evidence that they can work in concert. As

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2616168058768ad85f2eec8958db534
https://pubmed.ncbi.nlm.nih.gov/33249983

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Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3 -knock-in mice

Autor: Felix W. Friedrich, Silke Reischmann-Düsener, Frederik Flenner, Florian Weinberger, Lucie Carrier, Birgit Geertz, Thomas Eschenhagen

Publikováno v: The Journal of Physiology. 595:3987-3999

Left ventricular hypertrophy, diastolic dysfunction and fibrosis are main features of hypertrophic cardiomyopathy (HCM). Guidelines recommend β-adrenoceptor or Ca2+ channel antagonists as pharmacological treatment. The Ca2+ channel blocker diltiazem

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_________::82fc2a313e732cf48d432688e6605cf6
https://doi.org/10.1113/jp273769

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Activation of autophagy ameliorates cardiomyopathy in Mybpc3-targeted knockin mice

Autor: Silke Reischmann-Düsener, Jeffrey Robbins, Sonia R. Singh, Qinghang Meng, Hanna Osinska, Lucie Carrier, Birgit Geertz, Antonia T.L. Zech, Elisabeth Krämer, Jolanda van der Velden, Charles Redwood, Maksymilian Prondzynski, Saskia Schlossarek

Publikováno v: Singh, S R, Zech, A T L, Geertz, B, Reischmann-Düsener, S, Osinska, H, Prondzynski, M, Krämer, E, Meng, Q, Redwood, C, van der Velden, J, Robbins, J, Schlossarek, S & Carrier, L 2017, ' Activation of Autophagy Ameliorates Cardiomyopathy in Mybpc3-Targeted Knockin Mice ', Circulation. Heart failure, vol. 10, no. 10, e004140 . https://doi.org/10.1161/CIRCHEARTFAILURE.117.004140
Circulation. Heart failure, 10(10):e004140. Lippincott Williams and Wilkins

Background: Alterations in autophagy have been reported in hypertrophic cardiomyopathy (HCM) caused by Danon disease, Vici syndrome, or LEOPARD syndrome, but not in HCM caused by mutations in genes encoding sarcomeric proteins, which account for most

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7579aecefad22e9120495e8a43a2f015
https://doi.org/10.1161/circheartfailure.117.004140

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Activation of Autophagy Ameliorates Cardiomyopathy in

Autor: Sonia R, Singh, Antonia T L, Zech, Birgit, Geertz, Silke, Reischmann-Düsener, Hanna, Osinska, Maksymilian, Prondzynski, Elisabeth, Krämer, Qinghang, Meng, Charles, Redwood, Jolanda, van der Velden, Jeffrey, Robbins, Saskia, Schlossarek, Lucie, Carrier

Publikováno v: Circulation. Heart failure. 10(10)

Alterations in autophagy have been reported in hypertrophic cardiomyopathy (HCM) caused by Danon disease, Vici syndrome, or LEOPARD syndrome, but not in HCM caused by mutations in genes encoding sarcomeric proteins, which account for most of HCM case

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::23ca88400ae6965d98660dffe83234a1
https://pubmed.ncbi.nlm.nih.gov/29021349

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Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3-knock-in mice

Autor: Frederik, Flenner, Birgit, Geertz, Silke, Reischmann-Düsener, Florian, Weinberger, Thomas, Eschenhagen, Lucie, Carrier, Felix W, Friedrich

Publikováno v: The Journal of physiology. 595(12)

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac illness and can lead to diastolic dysfunction, sudden cardiac death and heart failure.Treatment of HCM patients is empirical and current pharmacological treatments are unable to s

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=pmid________::9d237b5bd0dba1fca2e9b80819e04c6c
https://pubmed.ncbi.nlm.nih.gov/28090637

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