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Figure 1 Catalytically inactive phosphoinositide-3 kinase (PI3K inact) overexpression normalizes ßAR kinase-1 (ßARK1)-associated PI3K activity in failing hearts from calsequestrin (CSQ) transgenic mice. (a) ßARK1-associated PI3K activity in cardiac membranes from wild type (WT) (n = 8), CSQ (n = 8), and CSQ/PI3K inact (n = 8) mouse hearts. *p < 0.001 CSQ vs. WT or CSQ/PI3K inact (analysis of variance with Neuman-Keuls correction); PI3K (b) or (c) activities were assayed from the cytosolic extracts of the same hearts. Left panels show representative PI3K assays; right panels show summary data. There was no significant increase in the activity of PI3K over WT levels in both CSQ or CSQ/PI3K inact (in CSQ 1.0 ± 0.3-fold, in CSQ/PI3K inact 0.7 ± 0.1-fold compared with WT). Ori = origin; PIP = phosphatidylinositol-mono-phosphate; PIP2 = phosphatidylinositol-bis-phosphate.
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