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. Author manuscript; available in PMC: 2016 Jun 4.
Published in final edited form as: Mol Cell. 2015 May 14;58(5):794–803. doi: 10.1016/j.molcel.2015.04.017

Figure 6. Male Cul4a−/− mice develop cardiac hypertrophy which is partially rescued by lose of one Grk2 allele.

Figure 6

(A) Deletion of Cul4a increases Grk2 protein in heart. The steady state levels of Grk2 protein were determined in five 10-week old littermate male mice by Western blotting.

(B) Male Cul4a−/− mice develop heart hypertrophy. 10-week-old littermate male mice were dissected and their hearts were analyzed by H&E staining.

(C) Male Cul4a−/− mice develop heart hypertrophy. The heart weights (HW) of 67 age-matched male mice of different genotypes were determined and normalized to the body weight (BW). The statistical significances of heart weight differences between different genotypes were determined by p value calculation as indicated.

(D, E) Cul4a−/−, but not Cul4a−/−;Grk2+/− male mice develop heart hypertrophy. The heart weights (HW) of age-matched 40 male mice of different genotypes were determined and normalized to the body weight (BW). The statistical significances of heart weight differences between different genotypes were determined by p value calculation as indicated.