ArticleBMC research notes2010
Mice lacking the Cβ subunit of PKA are resistant to angiotensin II-induced cardiac hypertrophy and dysfunction.
Article in BMC research notes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed.
- Protein Kinase A Is a Master Regulator of Physiological and Pathological Cardiac Hypertrophy.Circulation research · 2024Article
- S14-Phosphorylated RPN6 Mediates Proteasome Activation by PKA and Alleviates Proteinopathy.Circulation research · 2023Article
- Physiological and pathological roles of protein kinase A in the heart.Cardiovascular research · 2022Review
- PRKACB variants in skeletal disease or adrenocortical hyperplasia: effects on protein kinase A.Endocrine-related cancer · 2020Article
- Effect of endostatin overexpression on angiotensin II-induced cardiac hypertrophy in rats.Chinese medical journal · 2019Article
- The Catalytic SubunitJournal of the Endocrine Society · 2019Article
- Protein Kinase A as a Promising Target for Heart Failure Drug Development.Archives of medical research · 2018Review
- Article
- Soluble adenylyl cyclase: A novel player in cardiac hypertrophy induced by isoprenaline or pressure overload.PloS one · 2018Article
- Protein Kinase A (PKA) Phosphorylation of Shp2 Protein Inhibits Its Phosphatase Activity and Modulates Ligand Specificity.The Journal of biological chemistry · 2015Article
- UCR1C is a novel activator of phosphodiesterase 4 (PDE4) long isoforms and attenuates cardiomyocyte hypertrophy.Cellular signalling · 2015Article
- Interactions between the regulatory subunit of type I protein kinase A and p90 ribosomal S6 kinase1 regulate cardiomyocyte apoptosis.Molecular pharmacology · 2014Article
- The quality control theory of aging.Pathobiology of aging & age related diseases · 2014Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPKA is a ubiquitous, multi-subunit cellular kinase that regulates a number of different physiological responses in response to cAMP, including metabolism, cell division, and cardiac function. Numerous studies have implicated altered PKA signaling in cardiac dysfunction. Recently, it has been shown that mice lacking the catalytic β subunit of PKA (PKA Cβ) are protected from age-related problems such as weight gain and enlarged livers, and we hypothesized that these mice might also be resistant to cardiomyopathy.
findingsAngiotensin II (ang II) induced hypertension in both PKA Cβ null mice and their WT littermates. However, PKA Cβ null mice were resistant to a number of ang II-induced, cardiopathological effects observed in the WT mice, including hypertrophy, decreased diastolic performance, and enlarged left atria.
conclusionThe Cβ subunit of PKA plays an important role in angiotensin-induced cardiac dysfunction. The Cβ null mouse highlights the potential of the PKA Cβ subunit as a pharmaceutical target for hypertrophic cardiac disease.
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Registered trials
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