Evidence map›Paper›PMID 19055733›Full record

ArticleJournal of molecular signaling2008

G-protein-coupled receptor-associated A-kinase anchoring proteins AKAP5 and AKAP12: differential signaling to MAPK and GPCR recycling.

Jiangchuan Tao, Craig C Malbon

Open access · diamondAbstract read
In one paragraph

Article in Journal of molecular signaling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Role of A-Kinase Anchoring Protein 12 in the Central Nervous System.Journal of clinical neurology (Seoul, Korea) · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Epac Function and cAMP Scaffolds in the Heart and Lung.Journal of cardiovascular development and disease · 2018
    Review
  9. Calcineurin signaling in the heart: The importance of time and place.Journal of molecular and cellular cardiology · 2017
    Review
  10. Review
  11. A-kinase-anchoring proteins coordinate inflammatory responses to cigarette smoke in airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  12. Trafficking of β-Adrenergic Receptors: Implications in Intracellular Receptor Signaling.Progress in molecular biology and translational science · 2015
    Review
  13. Review
  14. Review
  15. Article
  16. Gravin orchestrates protein kinase A and β2-adrenergic receptor signaling critical for synaptic plasticity and memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  17. Article
  18. Article
  19. A-kinase anchoring proteins regulate compartmentalized cAMP signaling in airway smooth muscle.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jiangchuan TaoDepartment of Pharmacology, School of Medicine, Health Sciences Center, State University of New York at Stony Brook, Stony Brook, NY 11794-8651, USA. craig@pharm.stonybrook.edu.
Craig C Malbon
State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA-kinase Anchoring Protein AKAP5 and AKAP12 both dock to the beta2-adrenergic receptor, the former constitutively, the latter dynamically in response to activation of the receptor with agonist.

resultsIn the current work we analyze the ability of each AKAP to contribute to two downstream signaling events, the activation of mitogen-activate protein kinase and the resensitization/recycling of the internalized, desensitized beta2-adrenergic receptor to the cell membrane. Although both AKAP share a large number of docking partners in common (e.g., beta2-adrenergic receptor, protein kinases A and C, protein phosphatase-2B, and negatively-charged membrane phospholipids), AKAP5 and AKAP12 are shown to segregate with respect to activation of Erk1,2 and to resensitization/recycling of beta2-adrenergic receptor. A431 cells were found to highly express AKAP12, but little of AKAP5. HEK293 cells, in contrast, were found to highly express AKAP5, but little of AKAP12. Suppression of the expression of AKAP5 in either A431 cells or HEK293 cells leads to loss of the ability of the beta2-adrenergic receptor to activate Erk1,2. Suppression of the expression of AKAP12 in either cell line leads to loss of the ability of these cells to resensitize the beta2-adrenergic receptor.

conclusionKnock-down experiments of endogenous AKAP 5 and AKAP12 in two cell lines used commonly to study beta2-adrenergic receptor signaling clearly discriminate between the activation of mitogen-activated protein kinase (a downstream read-out solely mediated by AKAP5) and receptor recycling (a downstream read-out solely mediated by AKAP12).

Identifiers

PMID19055733
PMCPMC2621157
OpenAlexW2087223965

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.