ArticleMolecular endocrinology (Baltimore, Md.)2011
Differential role of PKA catalytic subunits in mediating phenotypes caused by knockout of the Carney complex gene Prkar1a.
Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Identification of Key Candidate Genes for Muscle Growth in Liaoning Black Pigs and Duroc Pigs via Longissimus Dorsi Muscle Transcriptome Analysis.Current issues in molecular biology · 2025Article
- Protein kinase A and local signaling in cancer.The Biochemical journal · 2024Review
- Discovery of a Cushing's syndrome protein kinase A mutant that biases signaling through type I AKAPs.Science advances · 2024Article
- Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.Circulation research · 2024Article
- Oncogenic PKA signaling increases c-MYC protein expression through multiple targetable mechanisms.eLife · 2023Article
- Evaluation of Protein Kinase cAMP-Activated Catalytic Subunit Alpha as a Therapeutic Target for Fibrolamellar Carcinoma.Gastro hep advances · 2023Article
- Germline and Mosaic Variants in PRKACA and PRKACB Cause a Multiple Congenital Malformation Syndrome.American journal of human genetics · 2020Article
- PRKACB variants in skeletal disease or adrenocortical hyperplasia: effects on protein kinase A.Endocrine-related cancer · 2020Article
- PRKAR1A deficiency impedes hypertrophy and reduces heart size.Physiological reports · 2020Article
- PKA Activates AMPK Through LKB1 Signaling in Follicular Thyroid Cancer.Frontiers in endocrinology · 2019Article
- Enhanced Integrin α4β1-Mediated Adhesion Contributes to a Mobilization Defect of Endothelial Progenitor Cells in Diabetes.Diabetes · 2016Article
- Studies of mice with cyclic AMP-dependent protein kinase (PKA) defects reveal the critical role of PKA's catalytic subunits in anxiety.Behavioural brain research · 2016Article
- Haploinsufficiency for either one of the type-II regulatory subunits of protein kinase A improves the bone phenotype of Prkar1a+/- mice.Human molecular genetics · 2015Article
- Mechanisms of cyclic AMP/protein kinase A- and glucocorticoid-mediated apoptosis using S49 lymphoma cells as a model system.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- E pluribus unum? The main protein kinase A catalytic subunit (PRKACA), a likely oncogene, and cortisol-producing tumors.The Journal of clinical endocrinology and metabolism · 2014Article
- Knockdown of PRKAR1A, the gene responsible for Carney complex, interferes with differentiation in osteoblastic cells.Molecular endocrinology (Baltimore, Md.) · 2014Article
- The role of genetic and epigenetic changes in pituitary tumorigenesis.Neurologia medico-chirurgica · 2014Review
- [Psammomatous melanotic schwannoma as indicator of a Carney complex].Der Pathologe · 2013Article
- cAMP/PKA signaling defects in tumors: genetics and tissue-specific pluripotential cell-derived lesions in human and mouse.Molecular and cellular endocrinology · 2013Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The Carney complex is an inherited tumor predisposition caused by activation of the cAMP-dependent protein kinase [protein kinase A (PKA)] resulting from mutation of the PKA-regulatory subunit gene PRKAR1A. Myxomas and tumors in cAMP-responsive tissues are cardinal features of this syndrome, which is unsurprising given the important role played by PKA in modulating cell growth and function. Previous studies demonstrated that cardiac-specific knockout of Prkar1a causes embryonic heart failure and myxomatous degeneration in the heart, whereas limited Schwann cell-specific knockout of the gene causes schwannoma formation. In this study, we sought to determine the role of PKA activation in this phenotype by using genetic means to reduce PKA enzymatic activity. To accomplish this goal, we introduced null alleles of the PKA catalytic subunits Prkaca (Ca) or Prkacb (Cb) into the Prkar1a-cardiac knockout (R1a-CKO) or limited Schwann cell knockout (R1a-TEC3KO) line. Heterozygosity for Prkaca rescued the embryonic lethality of the R1a-CKO, although mice had a shorter than normal lifespan and died from cardiac failure with atrial thrombosis. In contrast, heterozygosity for Prkacb only enabled the mice to survive 1 extra day during embryogenesis. Biochemical analysis indicated that reduction of Ca markedly reduced PKA activity in embryonic hearts, whereas reduction of Cb had minimal effects. In R1a-TEC3KO mice, tumorigenesis was completely suppressed by a heterozygosity for Prkaca, and by more than 80% by heterozygosity for Prkacb. These data suggest that both developmental and tumor phenotypes caused by Prkar1a mutation result from excess PKA activity due to PKA-Ca.
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