Protein phosphatase 5 regulates titin phosphorylation and function at a sarcomere-associated mechanosensor complex in cardiomyocytes

Autor: Judith Krysiak, Andreas Unger, Lisa Beckendorf, Nazha Hamdani, Marion von Frieling-Salewsky, Margaret M. Redfield, Cris G. dos Remedios, Farah Sheikh, Ulrich Gergs, Peter Boknik, Wolfgang A. Linke

Publikováno v: Nature Communications, Vol 9, Iss 1, Pp 1-14 (2018)

Protein phosphatase 5 (PP5) is expressed in many cell types but its role in cardiomyocytes is unknown. Here the authors show that PP5 binds and dephosphorylates elastic titin in cardiac sarcomeres, and that PP5 is increased in heart failure, reducing

Externí odkaz: https://doaj.org/article/cf31000b822e4204a0bb95e237b05a56

Crucial Role for Ca 2+ /Calmodulin-Dependent Protein Kinase-II in Regulating Diastolic Stress of Normal and Failing Hearts via Titin Phosphorylation

Autor: Michael M. Kreusser, Stefan Neef, Markus Krüger, Johannes Backs, Judith Krysiak, Wolfgang A. Linke, Nazha Hamdani, Lars S. Maier, Cristobal G. dos Remedios

Publikováno v: Hamdani, N, Krysiak, J, Kreusser, M M, Neef, S, dos Remedios, C G, Maier, L S, Kruger, M, Backs, J & Linke, W A 2013, ' Crucial Role for Ca2+/Calmodulin-Dependent Protein Kinase-II in Regulating Diastolic Stress of Normal and Failing Hearts via Titin Phosphorylation ', Circulation Research, vol. 112, no. 4, pp. 664-674 . https://doi.org/10.1161/CIRCRESAHA.111.300105
Circulation Research, 112(4), 664-674. Lippincott Williams and Wilkins

Rationale: Myocardial diastolic stiffness and cardiomyocyte passive force (F passive ) depend in part on titin isoform composition and phosphorylation. Ca 2+ /calmodulin-dependent protein kinase-II (CaMKII) phosphorylates ion channels, Ca 2+ -handlin

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c31a02cfc14bf68746f20342896276b7
https://doi.org/10.1161/circresaha.111.300105

Prevention of Myofilament Dysfunction by beta-Blocker Therapy in Postinfarct Remodeling

Autor: Lori A. Walker, Lucie Carrier, Daphne Merkus, Ger J.M. Stienen, Giulia Mearini, Amanda M. G. Versteilen, Judith Krysiak, Nicky M. Boontje, Wolfgang A. Linke, Jos M. J. Lamers, Vincent J. de Beer, Dirk J. Duncker, Ali El-Armouche, Jolanda van der Velden

Publikováno v: Duncker, D J, Boontje, N, Merkus, D, Versteilen, A M G, Krysiak, J, Mearini, G, El-Armouche, A, de Beer, V J, Lamers, J M J, Carrier, L, Walker, L A, Linke, W A, Stienen, G J M & van der Velden, J 2009, ' Prevention of myofilament dysfunction by beta-blocker therapy in postinfarct remodeling ', Circulation. Heart failure, vol. 2, no. 3, pp. 233-242 . https://doi.org/10.1161/CIRCHEARTFAILURE.108.806125
Circulation. Heart failure, 2(3), 233-242. Lippincott Williams and Wilkins
Circulation-Heart Failure, 2(3), 233-242. Lippincott Williams & Wilkins

Background— Myofilament contractility of individual cardiomyocytes is depressed in remote noninfarcted myocardium and contributes to global left ventricular pump dysfunction after myocardial infarction (MI). Here, we investigated whether β-blocker

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7eabe07a904cde3df241cf10a8e5eb1e
https://doi.org/10.1161/circheartfailure.108.806125

Multiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs

Autor: Judith Krysiak, Reza Wakili, Denis Chartier, Yanfen Shi, Peter Boknik, Jean-Claude Tardif, Gerrit J.M. Stienen, Kunihiro Nishida, Ulrich Schotten, Wolfgang A. Linke, Ange Maguy, Maura Greiser, Stanley Nattel, Stefan Kääb, Niels Voigt, Xiao Yan Qi, Yung-Hsin Yeh, Louis-Robert Villeneuve, Dobromir Dobrev, Ursula Ravens

Publikováno v: Wakili, R, Yeh, Y H, Qi, X A Y, Greiser, M, Chartier, D, Nishida, K, Maguy, A, Villeneuve, L R, Boknik, P, Voigt, N, Krysiak, J, Kaab, S, Ravens, U, Linke, W A, Stienen, G J M, Shi, Y F, Tardif, J C, Schotten, U, Dobrev, D & Nattel, S 2010, ' Multiple Potential Molecular Contributors to Atrial Hypocontractility Caused by Atrial Tachycardia Remodeling in Dogs ', Circulation. Arrhythmia and Electrophysiology, vol. 3, no. 5, pp. 530-541 . https://doi.org/10.1161/CIRCEP.109.933036
Circulation-Arrhythmia and Electrophysiology, 3(5), 530-U172. LIPPINCOTT WILLIAMS & WILKINS
Circulation. Arrhythmia and Electrophysiology, 3(5), 530-541. Lippincott Williams and Wilkins

Background— Atrial fibrillation impairs atrial contractility, inducing atrial stunning that promotes thromboembolic stroke. Action potential (AP)-prolonging drugs are reported to normalize atrial hypocontractility caused by atrial tachycardia remod

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9f412e161ed2b218a3da80994ca8588a
https://doi.org/10.1161/circep.109.933036

Crucial Role for Ca2+/Calmodulin-Dependent Protein Kinase-II Delta in Regulating Diastolic Stress of Normal and Failing Hearts via Titin Phosphorylation

Autor: Markus Krüger, Wolfgang A. Linke, Michael M. Kreusser, Cris dos Remedios, Lars S. Maier, Nazha Hamdani, Stefan Neef, Johannes Backs, Judith Krysiak

Publikováno v: Biophysical Journal. (2):18a

Rationale: Myocardial diastolic stiffness and cardiomyocyte passive force (Fpassive) depend in part on titin isoform composition and phosphorylation. Ca2+/calmodulin-dependent protein kinase-IIδ (CaMKIIδ) phosphorylates ion channels, Ca2+-handling

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::259ed10c048a944d129417e55297a8c7