Fig. 10 | Scientific Reports

Fig. 10

From: Desmoplakin CSM models unravel mechanisms regulating the binding to intermediate filaments and putative therapeutics for cardiocutaneous diseases

Fig. 10

Graphical summary detailing the key findings of this study placed in the physiological context of normal cardiac tissue remodeling and pathological setting of arrhythmogenic cardiomyopathy. This model is based on original structural data from PEP-FOLD de novo predictive modeling of wildtype and mutant R2834H DP CT tail (a.a. 2830–2865) as well as known in vitro data from previous studies9. PEP-FOLD-designed mutant DP CT tail was used for molecular docking in the virtual screening of FDA-approved drug librairies (PubChem, NIH) aiming to identify potential drug candidates for treatment of R2834H-induced cardiocutaneous diseases such as arrhythmogenic cardiomyopathy. Detailed explanations can be found in the “Discussion” section. PRD plakin repeat domain, P phosphorylation, Me methylation.

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