ArticleMolecular pharmacology2011
Beneficial effects of adenylyl cyclase type 6 (AC6) expression persist using a catalytically inactive AC6 mutant.
Article in Molecular pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Cardiac-directed expression of a catalytically inactive adenylyl cyclase 6 protects the heart from sustained β-adrenergic stimulation.PloS one · 2017Article
- Fine Tuning Adenylyl Cyclase as a (Gene) Therapy for Heart Failure.JACC. Basic to translational science · 2016Article
- Intravenous AAV8 Encoding Urocortin-2 Increases Function of the Failing Heart in Mice.Human gene therapy · 2015Article
- Cyclic AMP synthesis and hydrolysis in the normal and failing heart.Pflugers Archiv : European journal of physiology · 2014Review
- Non-raft adenylyl cyclase 2 defines a cAMP signaling compartment that selectively regulates IL-6 expression in airway smooth muscle cells: differential regulation of gene expression by AC isoforms.Naunyn-Schmiedeberg's archives of pharmacology · 2014Article
- Intravenous adeno-associated virus serotype 8 encoding urocortin-2 provides sustained augmentation of left ventricular function in mice.Human gene therapy · 2013Article
- Article
- Prospects for gene transfer for clinical heart failure.Gene therapy · 2012Review
- Choreographing the adenylyl cyclase signalosome: sorting out the partners and the steps.Naunyn-Schmiedeberg's archives of pharmacology · 2012Review
- Type VI adenylyl cyclase regulates neurite extension by binding to Snapin and Snap25.Molecular and cellular biology · 2011Article
- Methods in cardiomyocyte isolation, culture, and gene transfer.Journal of molecular and cellular cardiology · 2011Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac-directed expression of AC6 has pronounced favorable effects on cardiac function possibly not linked with cAMP production. To determine rigorously whether cAMP generation is required for the beneficial effects of increased AC6 expression, we generated a catalytically inactive AC6 mutant (AC6mut) that has markedly diminished cAMP generating capacity by replacing aspartic acid with alanine at position 426 in the C1 domain (catalytic region) of AC6. Gene transfer of AC6 or AC6mut (adenovirus-mediated) in adult rat cardiac myocytes resulted in similar expression levels and intracellular distribution, but AC6mut expression was associated with marked reduction in cAMP production. Despite marked reduction in cAMP generation, AC6mut influenced intracellular signaling events similarly to that observed after expression of catalytically intact AC6. For example, both AC6 and AC6mut reduced phenylephrine-induced cardiac myocyte hypertrophy and apoptosis (p < 0.001), expression of cardiac ankyrin repeat protein (p < 0.01), and phospholamban (p < 0.05). AC6mut expression, similar to its catalytically intact cohort, was associated with increased Ca2+ transients in cardiac myocytes after isoproterenol stimulation. Many of the biological effects of AC6 expression are replicated by a catalytically inactive AC6 mutant, indicating that the mechanisms for these effects do not require increased cAMP generation.
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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.