Letter concerning: 'Enhanced expression of DYRK1A in cardiomyocytes inhibits acute NFAT activation but does not prevent hypertrophy in vivo': reply

Abstract

We would like to thank da Costa Martins and De Windt for giving us the opportunity to discuss our recent paper in more detail.1 They state that ‘… a quantitative analysis of endogenous or transgenic Dyrk1a expression was not provided …’ and ‘… it remains unclear what level of overexpression over endogenous myocardial Dyrk1a was actually achieved by the transgenic system …’. The authors may have overlooked that we provide exactly this information in detail in our article: see Fig. 2A displaying the protein overexpression time course, see page 523 line 101 where we state that the level of overexpression was 5.1-fold, and see the quantitative real-time RT–PCR data on the level of Dyrk1a mRNA expression (see Supplementary material online, Figure S2B ). Furthermore, da Costa Martins and De Windt state that ‘… endogenous Rcan1 protein expression was not measured in the study by Grebe et al. ’ However, endogenous Rcan1–4 mRNA expression was indeed quantified in both the TAC and calcineurin transgenic disease models and is displayed in Fig. 4B . da Costa Martins and De Windt ask whether we observed alterations in endogenous DYRK1A expression following aortic banding or calcineurin co-expression. Although the data were not fully included in the paper (but see Supplementary material online, Figure S2C …