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4 results on '"Sickmann A"'

1. Aspartate signalling drives lung metastasis via alternative translation

Author

Doglioni, Ginevra, Fernández-García, Juan, Igelmann, Sebastian, Altea-Manzano, Patricia, Blomme, Arnaud, La Rovere, Rita, Liu, Xiao-Zheng, Liu, Yawen, Tricot, Tine, Nobis, Max, An, Ning, Leclercq, Marine, El Kharraz, Sarah, Karras, Panagiotis, Hsieh, Yu-Heng, Solari, Fiorella A., Martins Nascentes Melo, Luiza, Allies, Gabrielle, Scopelliti, Annalisa, Rossi, Matteo, Vermeire, Ines, Broekaert, Dorien, Ferreira Campos, Ana Margarida, Neven, Patrick, Maetens, Marion, Van Baelen, Karen, Alkan, H. Furkan, Planque, Mélanie, Floris, Giuseppe, Sickmann, Albert, Tasdogan, Alpaslan, Marine, Jean-Christophe, Scheele, Colinda L. G. J., Desmedt, Christine, Bultynck, Geert, Close, Pierre, and Fendt, Sarah-Maria

Published
2025
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2. From Ca2+ dysregulation to heart failure: β-adrenoceptor activation by RKIP postpones molecular damages and subsequent cardiac dysfunction in mice carrying mutant PLNR9C by correction of aberrant Ca2+-handling

Author

Brand, Theresa, Baumgarten, Bettina Tanitha, Denzinger, Sabrina, Reinders, Yvonne, Kleindl, Miriam, Schanbacher, Constanze, Funk, Florian, Gedik, Nilgün, Jabbasseh, Mahmood, Kleinbongard, Petra, Dudek, Jan, Szendroedi, Julia, Tolstik, Elen, Schuh, Kai, Krüger, Martina, Dobrev, Dobromir, Cuello, Friederike, Sickmann, Albert, Schmitt, Joachim P., and Lorenz, Kristina

Published
2025
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3. Analysis of differential gene expression of PBMC for the in vitrodetection of drug sensitization

Author

Glässner, Andreas, Steffens, Michael, Fatangare, Amol, Wurpts, Gerda, Hoffmann, Per, Deck, Philipp N., Krämer, Christine, Röseler, Stefani, Sickmann, Albert, Nöthen, Markus M., Yazdi, Amir S., and Sachs, Bernhardt

Abstract

The detection of drug-specific activation of T cells in the lymphocyte transformation test (LTT) is mainly based on cell proliferation or cytokine secretion. However, the LTT presents with a varying sensitivity and specificity. The aim of our study was to analyse the genome wide gene expression of PBMC to identify drug allergy-specific gene regulation patterns. Additionally, gene expression differences related to the allergy-inducing drug or the type of allergy (immediate/delayed) were investigated.

Published
2025
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4. From Ca2+ dysregulation to heart failure: β-adrenoceptor activation by RKIP postpones molecular damages and subsequent cardiac dysfunction in mice carrying mutant PLNR9C by correction of aberrant Ca2+-handling

Author

Theresa Brand, Bettina Tanitha Baumgarten, Sabrina Denzinger, Yvonne Reinders, Miriam Kleindl, Constanze Schanbacher, Florian Funk, Nilgün Gedik, Mahmood Jabbasseh, Petra Kleinbongard, Jan Dudek, Julia Szendroedi, Elen Tolstik, Kai Schuh, Martina Krüger, Dobromir Dobrev, Friederike Cuello, Albert Sickmann, Joachim P. Schmitt, and Kristina Lorenz

Subjects
Ca2+ dysregulation, Mitochondrial and ER defects, PLNR9C, RKIP, Heart failure, Therapeutics. Pharmacology, RM1-950
Abstract

Impaired cardiomyocyte Ca2+ handling is a central hallmark of heart failure (HF), which causes contractile dysfunction and arrhythmias. However, the underlying molecular mechanisms and the precise contribution of defects in Ca2+-cycling regulation in the development of HF are still not completely resolved. Here, we used transgenic mice that express a human mutation in the cardiomyocyte Ca2+-regulator phospholamban (PLNR9C-tg) causing severe HF due to a reduction in Ca2+ reuptake into the sarco(endo)plasmic reticulum (SR). PLNR9C-induced HF is a rapidly progressing condition characterized by prominent Ca2+ cycling and relaxation defects and premature death of mutation carriers. We found that endoplasmic reticulum (ER) and mitochondrial function are affected even before transition to overt HF. Early correction of aberrant Ca2+ cycling by cardiac expression of the Raf kinase inhibitor protein (RKIP), an endogenous activator of β-adrenoceptors (βAR), delayed the cellular alterations, functional failure and prolonged lifespan. Our study highlights the importance of early and persistent correction of Ca2 + dynamics, not only for excitation/contraction coupling, but also for the prevention of rather irreparable events on cardiac energetics and ER stress adaptations. The latter may even impede with later onset of Ca2+-related therapeutic interventions and should gain more focus for HF treatment.

Published
2025
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