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. Author manuscript; available in PMC: 2022 Jan 5.
Published in final edited form as: Endocr Relat Cancer. 2020 Nov;27(11):647–656. doi: 10.1530/ERC-20-0309

Figure 3. PKA activity in HEK293 cell lysates and immunohistochemistry in adrenal tissue from subject with p.T300M variant compared to controls.

Figure 3.

PKA activity was measured with co-expressed RIα (A) or RIIβ (B). The p.K286del variant had the highest baseline PKA activity, higher than p.S54L; unlike the p.S54L defect, the p.K286del failed to stimulate further upon exposure to cAMP. The p.T300M variant was not different from the baseline when co-expressed with RIα (A) or RIIβ (B). Data from 4 independent measurements are represented as mean ± SD and analyzed by two-way ANOVA with Tukey’s post hoc test for multiple comparisons, *P < 0.05 and ***P < 0.001 compared to basal Cβ wild-type (WT), ns stands for non-significant comparing the basal and the stimulated state (cAMP) of the same mutant. Representative Western Blots are indicated in Supplementary Figure 1. C. Adrenal tissue from the subject bearing the p.T300M variant expressed higher PRKACB protein with significant presence of phosphorylated CREB (p-CREB) compared to the adrenal gland from a PPNAD without PRKAR1A mutation. Magnification x40 of another immunostaining of PRKACB (D) and p-CREB presence (E) in the adrenal tissue of the subject bearing the p.T300M variant.