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Johannes Backs

Researcher at Heidelberg University

Publications -  146
Citations -  9119

Johannes Backs is an academic researcher from Heidelberg University. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Heart failure. The author has an hindex of 45, co-authored 126 publications receiving 7493 citations. Previous affiliations of Johannes Backs include University of Texas at Dallas & University Hospital Heidelberg.

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CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy

TL;DR: It is shown that calcium/calmodulin-dependent kinase II (CaMKII) signals specifically to HDAC4 by binding to a unique docking site that is absent in other class IIa HDACs, revealing a central role forHDAC4 in CaMKII signaling pathways and have implications for the control of gene expression by calcium signaling in a variety of cell types.
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Control of Cardiac Growth by Histone Acetylation/Deacetylation

TL;DR: Manipulation of histone modifying enzymes and the signaling pathways that impinge on them in the settings of pathological cardiac growth, remodeling, and heart failure represents an auspicious therapeutic approach.
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Calcium/calmodulin-dependent protein kinase II links ER stress with Fas and mitochondrial apoptosis pathways

TL;DR: It is shown that cytosolic calcium resulting from ER stress induces expression of the Fas death receptor through a pathway involving calcium/calmodulin-dependent protein kinase IIgamma (CaMKIIgamma) and JNK, and these findings raise the possibility that CaMKII inhibitors could be useful in preventing apoptosis in pathological settings involving ER stress-induced apoptosis.
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Histone deacetylase degradation and MEF2 activation promote the formation of slow-twitch myofibers.

TL;DR: The selective degradation of class II HDACs in slow skeletal muscle provides a mechanism for enhancing physical performance and resistance to fatigue by augmenting the transcriptional activity of MEF2.