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Enhanced Heart Failure in Redox‐Dead Cys17Ser PKARIα Knock‐In Mice

URN to cite this document:
urn:nbn:de:bvb:355-epub-516604
DOI to cite this document:
10.5283/epub.51660
Islam, M. M. Towhidul ; Tarnowski, Daniel ; Zhang, Min ; Trum, Maximilian ; Lebek, Simon ; Mustroph, Julian ; Daniel, Henriette ; Moellencamp, Johanna ; Pabel, Steffen ; Sossalla, Samuel ; El‐Armouche, Ali ; Nikolaev, Viacheslav O. ; Shah, Ajay M. ; Eaton, Philip J. ; Maier, Lars S. ; Sag, Can Martin ; Wagner, Stefan
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License: Creative Commons Attribution Non-commercial 4.0
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Date of publication of this fulltext: 14 Feb 2022 18:18


Abstract

Background PKARIα (protein kinase A type I‐α regulatory subunit) is redox‐active independent of its physiologic agonist cAMP. However, it is unknown whether this alternative mechanism of PKARIα activation may be of relevance to cardiac excitation–contraction coupling. Methods and Results We used a redox‐dead transgenic mouse model with homozygous knock‐in replacement of redox‐sensitive ...

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