ReviewCells2026
The Role of A-Kinase Anchoring Proteins for Inhibitory cAMP Signalling in Platelets.
Review in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Platelets are small circulating blood cells that mediate haemostasis and thrombosis. Platelets respond to vascular damage by adhesion, granule release, and aggregation. Healthy endothelial cells inhibit platelets through prostacyclin-induced cAMP signalling. Intracellular cAMP activates protein kinase A (PKA), a tetrameric kinase composed of two regulatory (R) and two catalytic (C) subunits. cAMP-binding triggers dissociation of C subunits from the PKA complex and phosphorylation of substrate proteins, which mediate platelet inhibition. The R subunits of PKA are known to be attached to A-kinase anchoring proteins (AKAPs), which enable subcellular compartmentalisation of cAMP signalling. Proteomics have identified 22 AKAPs in platelets, but only a few of these have been studied in detail. This review summarises current knowledge about platelet AKAPs, including studies done regarding other cells. Possible integration of AKAPs into platelet signalling is explored with a focus on subcellular localisation, interaction partners, and PKA-mediated substrate phosphorylation. As main platelet compartments, the plasma membrane, endosomes, mitochondria, the Golgi, the dense tubular system, and the cytoskeleton are considered. Potential roles of individual AKAPs in platelet inhibition are discussed, and open questions in the field are defined.
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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 Socratic graph.