Evidence map›Paper›PMID 25348485›Full record

ArticleProtein science : a publication of the Protein Society2015

D-AKAP2:PKA RII:PDZK1 ternary complex structure: insights from the nucleation of a polyvalent scaffold.

Ganapathy N Sarma, Issa S Moody, Ronit Ilouz, Ryan H Phan, Banumathi Sankaran, Randy A Hall, Susan S Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Protein science : a publication of the Protein Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. NaPi-IIa interacting partners and their (un)known functional roles.Pflugers Archiv : European journal of physiology · 2019
    Review
  7. MAP17 Is a Necessary Activator of Renal Na+/Glucose Cotransporter SGLT2.Journal of the American Society of Nephrology : JASN · 2017
    Article
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

7 authors at 4 institutions in 1 country.

Ganapathy N SarmaDepartment of Chemistry and Biochemistry, University of California, San Diego, La Jolla, California, 92093-0654; Department of Pharmacology, University of California, San Diego, La Jolla, California, 92093-0654.
Issa S Moody
Ronit Ilouz
Ryan H Phan
Banumathi Sankaran
Randy A Hall
Susan S Taylor
University of California, San Diego · USEmory University · USInformation Today (United States) · USLawrence Berkeley National Laboratory · US

Funding

Project# 4: INTERACTIONS OF ANCHORING PROTEINS WITH THEIR TARGETSP01DK054441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR, SUSAN S. · 1999 to 2017
$27.3M
Protein Kinase Regulatory Subunit I Directed MutagenesisR01GM034921 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR, SUSAN S. · 1985 to 2018
$7.2M
NIDDK NIH HHS DK054441NIDDK NIH HHS P01 DK054441NIGMS NIH HHS GM34921NIGMS NIH HHS R01 GM034921
6 · The paper itself

Abstract

A-kinase anchoring proteins (AKAPs) regulate cAMP-dependent protein kinase (PKA) signaling in space and time. Dual-specific AKAP2 (D-AKAP2/AKAP10) binds with high affinity to both RI and RII regulatory subunits of PKA and is anchored to transporters through PDZ domain proteins. Here, we describe a structure of D-AKAP2 in complex with two interacting partners and the exact mechanism by which a segment that on its own is disordered presents an α-helix to PKA and a β-strand to PDZK1. These two motifs nucleate a polyvalent scaffold and show how PKA signaling is linked to the regulation of transporters. Formation of the D-AKAP2: PKA binary complex is an important first step for high affinity interaction with PDZK1, and the structure reveals important clues toward understanding this phenomenon. In contrast to many other AKAPs, D-AKAP2 does not interact directly with the membrane protein. Instead, the interaction is facilitated by the C-terminus of D-AKAP2, which contains two binding motifs-the D-AKAP2AKB and the PDZ motif-that are joined by a short linker and only become ordered upon binding to their respective partner signaling proteins. The D-AKAP2AKB binds to the D/D domain of the R-subunit and the C-terminal PDZ motif binds to a PDZ domain (from PDZK1) that serves as a bridging protein to the transporter. This structure also provides insights into the fundamental question of why D-AKAP2 would exhibit a differential mode of binding to the two PKA isoforms.

Indexed as

A Kinase Anchor ProteinsAmino Acid SequenceAnimalsCarrier ProteinsCrystallography, X-RayCyclic AMP-Dependent Protein Kinase RIalpha SubunitHumansMembrane ProteinsModels, MolecularMolecular Sequence DataPDZ DomainsProtein ConformationRatsAKAP10 protein, humanA Kinase Anchor ProteinsCarrier ProteinsCyclic AMP-Dependent Protein Kinase RIalpha SubunitMembrane ProteinsPDZK1 protein, humanPrkar1a protein, ratAKAP10A-kinase anchoring proteinsD-AKAP2 specificityPDZK1 crystal structurePKA signaling

Identifiers

PMID25348485
PMCPMC4282416
OpenAlexW2171521993

What OpenQuestion holds

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Registered trials

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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.