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Editorial
. 2017 Apr 1;113(5):437-439.
doi: 10.1093/cvr/cvx041.

Modelling human calmodulinopathies with induced pluripotent stem cells: progress and challenges

Nieves Gomez-Hurtado, Daniel Jesse Blackwell, Bjorn Christian Knollmann
Editorial

Modelling human calmodulinopathies with induced pluripotent stem cells: progress and challenges

Nieves Gomez-Hurtado et al. Cardiovasc Res. .
No abstract available

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Figures

Figure 1
Figure 1
Cartoon of a ventricular cardiomyocyte. Calmodulin (CaM) regulates many important proteins involved in excitation-contraction coupling and calcium homeostasis. The proteins interacting with red F142L-CaM are those examined in the study by Rocchetti et al. Protein interactions with blue F142L-CaM were investigated in previous studies, whereas grey F142L-CaM indicates targets that have not yet been characterized in the context of this mutant. The findings from these studies are illustrated by an increase (↑), decrease (↓), or no change (=) in the respective activity of these proteins. The numbers in brackets correspond to the bibliographic reference in which a particular target was studied. Note that calcium-dependent inactivation of L-type calcium current (CDI ICaL) is decreased. IKCa, calcium activated potassium current; PMCA, plasma membrane calcium ATPase; IKs, delayed rectifier potassium current; INa, sodium current; RyR2, cardiac ryanodine receptor; CaMKII, Ca2+/CaM-dependent protein kinase II; PDE1, phosphodiesterase type 1.
See this image and copyright information in PMC

Comment on

References

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