Fig. 3: Protein kinase A (PKA) activity and PRKAR1B subunit expression in tumors with 7p22 copy-number gain (CNG). | Genetics in Medicine

Fig. 3: Protein kinase A (PKA) activity and PRKAR1B subunit expression in tumors with 7p22 copy-number gain (CNG).

From: Genomic and sequence variants of protein kinase A regulatory subunit type 1β (PRKAR1B) in patients with adrenocortical disease and Cushing syndrome

Fig. 3: Protein kinase A (PKA) activity and PRKAR1B subunit expression in tumors with 7p22 copy-number gain (CNG).The alternative text for this image may have been generated using AI.

(a) Tumor sample ADT35.02. (b) Tumor sample ADT47.03. (c) Detection of 7p22 CNG, by the hs04981093 probe, in tumors ADT35.02, ADT47.03, and ADT183.02 at positions 10, 12, and 17 respectively. (d) PKA activity was measured in tumor cell lysates. The three tumors with 7p22 CNG had lower basal PKA activity (in absence of cAMP, left panel) but no differences in total PKA activity (in presence of cAMP, right panel) from normal (NL) cortisol-producing adrenal adenomas (CPA) (N = 5) that did not contain 7p22 CNG. (e) The three CPAs with 7p22 CNG showed higher expression of the PRKAR1B messenger RNA (mRNA) compared with the five CPAs that were genomically NL. Asterisk (*) corresponds to tumor ADT47.03 as this is the CPA that also carried the L206R PRKACA “hotspot” pathogenic variant.

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