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. 2023 Jan 24;12:e69521. doi: 10.7554/eLife.69521

Figure 1. Recurrent PKA activating somatic alterations in human cancer.

Figure 1.

(A) Pathway illustrations of different PKA activating genomic alterations in order from top: PRKACA amplification, DNAJB1-PRKACA fusion, PRKACA activating mutation, and PRKAR1A inactivation or deletion. (B) TCGA PanCancer Project analysis showing the frequency of PRKACA gain-of-function (red and yellow) and PRKAR1A loss-of-function (green and blue) alterations in various cancer types. The reported frequency of DNAJB1-PRKACA fusion in fibrolamellar carcinoma (FLC) clinical samples is also included. (C) Cell lines used in this study, their PKA-related mutation, PRKACA dependency, and inclusion in proteomic analyses. (D) Immunoblots showing the change of PKA activity, as indicated by phospho-PKA substrate, in different cell lines with dox-inducible 3xFLAG-PRKACA or PRKAR1AG325D with 1 µg/ml doxycycline (dox) for 48 hr. Left: engineered cell lines with inducible 3xFLAG-PRKACA. Right: engineered cell lines with inducible 3xFLAG- PRKAR1AG325D.

Figure 1—source data 1. Images for Figure 1A.
Figure 1—source data 2. Table for Figure 1B.
Figure 1—source data 3. Images for Figure 1D part 1/3.
Figure 1—source data 4. Images for Figure 1D part 2/3.
Figure 1—source data 5. Images for Figure 1D part 3/3.