CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy
J. Clin. Invest. Johannes Backs, et al. 116:1853 doi:10.1172/JCI27438 [Go to this article.]

Figure 1
Selective response of HDAC4 to CaMKII. (A and B) COS cells were transfected with GFP-HDAC4, GFP-HDAC5, FLAG-HDAC7, or GFP-MITR together with either an empty vector (pcDNA), constitutively active (c.a.) CaMKI, PKD1 (c.a.), CaMKIIδB-T287D, CaMKIIδC-T287D, or CaMKIIγA-T287D. CaMKI c.a. induced nuclear export of all HDACs and changed the predominant nuclear localization of MITR from punctate to homogenous. CaMKIIδB-T287D and CaMKIIγA-T287D selectively induced cytosolic accumulation of HDAC4 but did not affect the subcellular distribution of HDAC5, HDAC7, and MITR. (A) Representative images. Magnification, ×40. (B) Quantitative analysis. (C) Coimmunoprecipitation assays with COS cell lysates were analyzed with an antibody directed against endogenous (endog.) 14-3-3 protein. HDAC-input, HDAC4 and -5 present in the COS cell lysate before IP was performed; Kinase-input, CaMKI, PKD1, or CaMKIIδB-T287D present in the COS cell lysate before IP was performed.