Skip to main content
. 2014 Apr 7;155(7):2524–2533. doi: 10.1210/en.2013-1485

Figure 5.

Figure 5.

The constitutively active Ser738/742-to-glutamate PKD mutant promoted, and the dominant-negative Ser738/742-to-alanine PKD mutant inhibited, AngII-induced CREB and ATF-2 phosphorylation. Cultured primary bovine glomerulosa cells were incubated for 4 hours with adenovirus expressing pAdtrackCMV (empty vector), or the Ser738/742-to-alanine (PKDS738/742A) or Ser738/742-to-glutamate (PKDS738/742E) PKD mutants. On the second day of culture, media were replaced with serum-free media for an additional 16–20 hours before treatment with or without AngII (10nM) for 1 hour. A, Representative blot. B and C, Band intensities from multiple experiments were quantified and normalized to their respective total proteins (TotCREB or TotATF-2), CREB (B) and ATF-2 (C). Analysis was performed on transformed data, and values were expressed relative to the maximal response (PKDS738/742E + AngII) as described in Materials and Methods. Values represent the means ± SEM from 4 experiments performed in duplicate; *, P < .05 vs control (vector); ***, P < .001 vs control (vector); †, P < .05 vs vector + AngII; †††, P < .001 vs vector + AngII; f, P < .05 vs PKDS738/742A + AngII; fff, P < .001 vs PKDS738/742A + AngII.