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- URN to cite this document:
- urn:nbn:de:bvb:355-epub-520580
- DOI to cite this document:
- 10.5283/epub.52058
Bengel, Philipp 
; Dybkova, Nataliya ; Tirilomis, Petros ; Ahmad, Shakil ; Hartmann, Nico ; A. Mohamed, Belal ; Krekeler, Miriam Celine ; Maurer, Wiebke ; Pabel, Steffen ; Trum, Maximilian ; Mustroph, Julian ; Gummert, Jan ; Milting, Hendrik ; Wagner, Stefan ; Ljubojevic-Holzer, Senka ; Toischer, Karl ; Maier, Lars S. ; Hasenfuss, Gerd ; Streckfuss-Bömeke, Katrin ; Sossalla, Samuel
; Dybkova, Nataliya ; Tirilomis, Petros ; Ahmad, Shakil ; Hartmann, Nico ; A. Mohamed, Belal ; Krekeler, Miriam Celine ; Maurer, Wiebke ; Pabel, Steffen ; Trum, Maximilian ; Mustroph, Julian ; Gummert, Jan ; Milting, Hendrik ; Wagner, Stefan ; Ljubojevic-Holzer, Senka ; Toischer, Karl ; Maier, Lars S. ; Hasenfuss, Gerd ; Streckfuss-Bömeke, Katrin ; Sossalla, Samuel 
Abstract
In heart failure, increased CaMKII activity is decisively involved in arrhythmia formation. Here, the authors introduce the neuronal sodium channel Na(V)1.8 as a CaMKII downstream target as its specific knock-out reduces arrhythmias and improves survival in a CaMKII-overexpressing mouse model. An interplay between Ca2+/calmodulin-dependent protein kinase II delta c (CaMKII delta c) and late Na+ ...
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