Evidence map›Paper›PMID 21561082›Full record

ArticleBiochemistry2011

Identification of AKAP79 as a protein phosphatase 1 catalytic binding protein.

Andrew V Le, Steven J Tavalin, Kimberly L Dodge-Kafka

Open access · greenAbstract read
In one paragraph

Article in Biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. cAMP regulation of protein phosphatases PP1 and PP2A in brain.Biochimica et biophysica acta. Molecular cell research · 2019
    Review
  5. Article
  6. Article
  7. Protein Phosphatase-1 Inhibitor-2 Is a Novel Memory Suppressor.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. A-kinase anchoring protein 9 and IKs channel regulation.Journal of cardiovascular pharmacology · 2011
    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

3 authors at 2 institutions in 1 country.

Andrew V LeUniversity of Connecticut Health Center, Farmington, CT 06030, USA.
Steven J Tavalin
Kimberly L Dodge-Kafka
UConn Health · USUniversity of Tennessee Health Science Center · US

Funding

mAKAP-orchestrated phosphorylation events: regulation of PDE4D3R01HL082705 · NHLBI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI DODGE-KAFKA, KIMBERLY L · 2006 to 2010
$1.8M
Regulation of Ionotropic Glutamate ReceptorsR01NS046661 · NINDS · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TAVALIN, STEVEN J · 2005 to 2008
$915k
NHLBI NIH HHS HL82705NHLBI NIH HHS R01 HL082705NINDS NIH HHS NS046661NINDS NIH HHS R01 NS046661
6 · The paper itself

Abstract

The ubiquitously expressed and highly promiscuous protein phosphatase 1 (PP1) regulates many cellular processes. Targeting PP1 to specific locations within the cell allows for the regulation of PP1 by conferring substrate specificity. In the present study, we identified AKAP79 as a novel PP1 regulatory subunit. Immunoprecipitaiton of the AKAP from rat brain extract found that the PP1 catalytic subunit copurified with the anchoring protein. This is a direct interaction, demonstrated by pulldown experiments using purified proteins. Interestingly, the addition of AKAP79 to purified PP1 catalytic subunit decreased phosphatase activity with an IC(50) of 811 ± 0.56 nM of the anchoring protein. Analysis of AKAP79 identified a PP1 binding site that conformed to a consensus PP1 binding motif (FxxR/KxR/K) in the first 44 amino acids of the anchoring protein. This was confirmed when a peptide mimicking this region of AKAP79 was able to bind PP1 by both pulldown assay and surface plasmon resonance. However, PP1 was still able to bind to AKAP79 upon deletion of this region, suggesting additional sites of contact between the anchoring protein and the phosphatase. Importantly, this consensus PP1 binding motif was found not to be responsible for PP1 inhibition, but rather enhanced phosphatase activity, as deletion of this domain resulted in an increased inhibition of PP1 activity. Instead, a second interaction domain localized to residues 150-250 of AKAP79 was required for the inhibition of PP1. However, the inhibitory actions of AKAP79 on PP1 are substrate dependent, as the anchoring protein did not inhibit PP1 dephosphorylation of phospho-PSD-95, a substrate found in AKAP79 complexes in the brain. These combined observations suggest that AKAP79 acts as a PP1 regulatory subunit that can direct PP1 activity toward specific targets in the AKAP79 complex.

Indexed as

A Kinase Anchor ProteinsAmino Acid SequenceAnimalsBinding SitesCatalysisCells, CulturedMolecular Sequence DataProtein Phosphatase 1Protein Structure, TertiaryRatsSurface Plasmon ResonanceAKAP5 protein, humanA Kinase Anchor ProteinsProtein Phosphatase 1

Identifiers

PMID21561082
PMCPMC3115558
OpenAlexW2026691793

What OpenQuestion holds

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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.