Evidence map›Paper›PMID 25654263›Full record

ArticleBiochemistry2015

How the ankyrin and SOCS box protein, ASB9, binds to creatine kinase.

Deepa Balasubramaniam, Jamie Schiffer, Jonathan Parnell, Stephan P Mir, Rommie E Amaro, Elizabeth A Komives

Abstract read
In one paragraph

Article in Biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Morphine Binds Creatine Kinase B and Inhibits Its Activity.Frontiers in cellular neuroscience · 2018
    Article
  6. Article
  7. Article
  8. Article
  9. 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

6 authors at 1 institution in 1 country.

Deepa BalasubramaniamDepartment of Chemistry and Biochemistry, University of California, San Diego , 9500 Gilman Drive, La Jolla, California 92093-0378, United States.
Jamie Schiffer
Jonathan Parnell
Stephan P Mir
Rommie E Amaro
Elizabeth A Komives
University of California, San Diego · US

Funding

STRUCTURE AND STABILITY OF IKB/NF-KB COMPLEXESP01GM071862 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HOFFMANN, ALEXANDER · 2006 to 2016
$14.9M
National Biomedical Computation Resource - Competitive Revision SupplementP41GM103426 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AMARO, ROMMIE E · 2012 to 2019
$14.0M
MOLECULAR BIOPHYSICS TRAINING PROGRAMT32GM008326 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOMIVES, ELIZABETH A. · 1989 to 2020
$7.5M
A Structural Systems Biology Approach to Drug DiscoveryDP2OD007237 · OD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI AMARO, ROMMIE E · 2010 to 2015
$2.9M
NIGMS NIH HHS P01 GM071862NIGMS NIH HHS P41 GM103426NIGMS NIH HHS T32 GM008326NIGMS NIH HHS T32 GM008326-23NIH HHS DP2 OD007237NIH HHS DP2-OD007237
6 · The paper itself

Abstract

The ankyrin repeat and SOCS box (ASB) family is composed of 18 proteins and belongs to the suppressor of cytokine signaling (SOCS) box protein superfamily. The ASB proteins function as the substrate-recognition subunits of ECS-type (ElonginBC-Cullin-SOCS-box) Cullin RING E3 ubiquitin ligase (CRL) complexes that specifically transfer ubiquitin to cellular proteins targeting them for degradation by the proteasome. ASB9 binds to creatine kinase (CK) and targets it for degradation; however, the way in which ASB9 interacts with CK is not yet known. We present a complete characterization of the binding of ASB9 to CK. One ASB9 molecule binds to a dimer of CK. The binding affinity of ASB9(1-252) was extremely tight, and no dissociation could be observed. Deletion of the 34 N-terminal amino acids forming ASB9(35-252) resulted in weakening of the binding, so that a binding affinity of 2.6 nM could be measured. Amide hydrogen-deuterium exchange (HDXMS) experiments showed that both ASB9(1-252) and ASB9(35-252) protected the same region of CK, residues 182-203, which forms one side of the active site. The HDXMS experiments indicated that the N-terminal disordered region and first ankyrin repeat of ASB9 are protected from exchange in the complex. Molecular docking yielded a structural model consistent with all of the data that suggested the N-terminal residues of ASB9(1-252) may lie in one CK active site. This model was corroborated by enzymatic activity assays and mutational analysis.

Indexed as

Molecular Docking SimulationAmino Acid SequenceCreatine KinaseDeuterium Exchange MeasurementHumansProtein BindingProteolysisSequence DeletionSuppressor of Cytokine Signaling ProteinsASB9 protein, humanCreatine KinaseSuppressor of Cytokine Signaling Proteins

Identifiers

PMID25654263
PMCPMC4348336
OpenAlexW2323525755

What OpenQuestion holds

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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.