ReviewCurrent opinion in endocrinology, diabetes, and obesity2015
Protein kinase A defects and cortisol-producing adrenal tumors.
Review in Current opinion in endocrinology, diabetes, and obesity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Molecular Basis Underlying Changes of Brain Entropy and Couplings in Late-life Depression.Current neuropharmacology · 2026Article
- A Bibliometric Analysis and Visualization of the Current Status and Future Perspectives of Adrenal Cortical Adenoma.Cureus · 2025Review
- Adrenal hyperplasias in childhood: An update.Frontiers in endocrinology · 2022Review
- β-catenin in adrenal zonation and disease.Molecular and cellular endocrinology · 2021Review
- Cushing's Syndrome in Pediatrics: An Update.Endocrinology and metabolism clinics of North America · 2018Review
- Gpr161 anchoring of PKA consolidates GPCR and cAMP signaling.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Diagnosis and Clinical Genetics of Cushing Syndrome in Pediatrics.Endocrinology and metabolism clinics of North America · 2016Review
- Impact of kinase activating and inactivating patient mutations on binary PKA interactions.Frontiers in pharmacology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
purpose of reviewCushing syndrome caused by cortisol-producing adrenal adenomas is a rare condition, associated with high morbidity due to weight gain, diabetes mellitus, osteoporosis, hypertension, muscle weakness, mood disturbance and others. The first gene to be identified as causative of Cushing syndrome was PRKAR1A. We present an update on protein kinase A (PKA) defects and Cushing syndrome. RECENT
findingsThe cyclic AMP-dependent PKA catalytic subunit alpha (PRKACA) hotspot point mutation (c.617A > C [p.Leu206Arg]), leading to an increase of basal PKA activity, and formation of cortisol-producing adenoma has been frequently shown to cause the most common form of adrenocorticotropic hormone-independent Cushing syndrome. SUMMARY: Somatic PRKACA mutations have been found in up to 50% of patients with adrenal adenomas. Germline PRKACA amplification was also seen in bilateral adrenal hyperplasias. PRKACA activation was associated with higher cortisol levels, smaller tumor size and overt Cushing syndrome. This breakthrough is expected to improve our understanding of how PKA defects lead to Cushing syndrome and may spearhead the development of new, molecularly designed therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.