Evidence map›Paper›PMID 21699177›Full record

ArticleBiochemistry2011

Defining the substrate specificity determinants recognized by the active site of C-terminal Src kinase-homologous kinase (CHK) and identification of β-synuclein as a potential CHK physiological substrate.

Kim K Ia, Grace R Jeschke, Yang Deng, Mohd Aizuddin Kamaruddin, Nicholas A Williamson, Denis B Scanlon, Janetta G Culvenor, Mohammed Iqbal Hossain, Anthony W Purcell, Sheng Liu and 4 more

Abstract readComparative Study
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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Regulation, targets and functions of CHK.Frontiers in cell and developmental biology · 2022
    Review
  4. Article
  5. Article
  6. 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

14 authors at 3 institutions in 2 countries.

Kim K IaDepartment of Biochemistry and Molecular Biology, University of Melbourne, Parkville, Victoria 3010, Australia.
Grace R Jeschke
Yang Deng
Mohd Aizuddin Kamaruddin
Nicholas A Williamson
Denis B Scanlon
Janetta G Culvenor
Mohammed Iqbal Hossain
Anthony W Purcell
Sheng Liu
Hong-Jian Zhu
Bruno Catimel
Benjamin E Turk
Heung-Chin Cheng
University of Melbourne · AUYale University · USThe Royal Melbourne Hospital · AU

Funding

Proteome-wide analysis of kinase phosphorylation specificity in yeastR01GM079498 · NIGMS · YALE UNIVERSITY · PI TURK, BENJAMIN E · 2007 to 2011
$1.8M
Global peptide microarray profiling of tyrosine kinases deregulated in cancerR21CA147993 · NCI · YALE UNIVERSITY · PI TURK, BENJAMIN E · 2010 to 2011
$349k
NCI NIH HHS R21 CA147993NIGMS NIH HHS R01 GM079498
6 · The paper itself

Abstract

C-Terminal Src kinase-homologous kinase (CHK) exerts its tumor suppressor function by phosphorylating the C-terminal regulatory tyrosine of the Src-family kinases (SFKs). The phosphorylation suppresses their activity and oncogenic action. In addition to phosphorylating SFKs, CHK also performs non-SFK-related functions by phosphorylating other cellular protein substrates. To define these non-SFK-related functions of CHK, we used the "kinase substrate tracking and elucidation" method to search for its potential physiological substrates in rat brain cytosol. Our search revealed β-synuclein as a potential CHK substrate, and Y127 in β-synuclein as the preferential phosphorylation site. Using peptides derived from β-synuclein and positional scanning combinatorial peptide library screening, we defined the optimal substrate phosphorylation sequence recognized by the CHK active site to be E-x-[Φ/E/D]-Y-Φ-x-Φ, where Φ and x represent hydrophobic residues and any residue, respectively. Besides β-synuclein, cellular proteins containing motifs resembling this sequence are potential CHK substrates. Intriguingly, the CHK-optimal substrate phosphorylation sequence bears little resemblance to the C-terminal tail sequence of SFKs, indicating that interactions between the CHK active site and the local determinants near the C-terminal regulatory tyrosine of SFKs play only a minor role in governing specific phosphorylation of SFKs by CHK. Our results imply that recognition of SFKs by CHK is mainly governed by interactions between motifs located distally from the active site of CHK and determinants spatially separate from the C-terminal regulatory tyrosine in SFKs. Thus, besides assisting in the identification of potential CHK physiological substrates, our findings shed new light on how CHK recognizes SFKs and other protein substrates.

Indexed as

src Homology DomainsStructural Homology, ProteinAmino Acid MotifsAmino Acid SequenceAnimalsbeta-SynucleinCatalytic DomainCSK Tyrosine-Protein KinaseCytosolHEK293 CellsHumansMolecular Sequence DataPeptide LibraryPhosphorylationProtein-Tyrosine KinasesRatsbeta-SynucleinCSK protein, humanCSK Tyrosine-Protein KinasePeptide LibraryProtein-Tyrosine Kinasessrc-Family Kinases

Identifiers

PMID21699177
PMCPMC3156789
OpenAlexW2052976240

What OpenQuestion holds

Textmetadata
LicenceTDM
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.