Skip to main content
. Author manuscript; available in PMC: 2010 Feb 1.
Published in final edited form as: Trends Cardiovasc Med. 2009 Feb;19(2):44–49. doi: 10.1016/j.tcm.2009.04.005

Figure 1. Model for the interactions of Prkar1a with other genes sharing a cardiac phenotype.

Figure 1

Prkar1a KO (red text) causes reduction of cardiac-specific genes and a reduced number of cardiomyocytes with aberrant sarcomeres (Middle figure: white arrow: residual Z-disk; arrowhead: residual I-band)), eventually leading to a thin-walled, dilated heart (Right figure). At the end, these changes cause myxomagenesis (Left figure, arrows), and embryonic demise. These same pathways may be affected by knockout of other cardiac-specific transcription factors (blue text). A mechanism to account for myxomagenesis associated with mutation of MYH8 is also proposed in the same scheme. See text for details and references.