Evidence map›Paper›PMID 21263009›Full record

ArticleMolecular & cellular proteomics : MCP2011

A screen for novel phosphoinositide 3-kinase effector proteins.

Miles J Dixon, Alexander Gray, François-Michel Boisvert, Mark Agacan, Nicholas A Morrice, Robert Gourlay, Nicholas R Leslie, C Peter Downes, Ian H Batty

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. In-depth PtdIns(3,4,5)PBlood advances · 2017
    Article
  4. Review
  5. IQGAP1 is a phosphoinositide effector and kinase scaffold.Advances in biological regulation · 2016
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
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  14. Article
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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

9 authors at 2 institutions in 1 country.

Miles J DixonThe Division of Molecular Physiology, College of Life Sciences, University of Dundee, Dow St., Dundee, DD1 5EH, Scotland, UK.
Alexander Gray
François-Michel Boisvert
Mark Agacan
Nicholas A Morrice
Robert Gourlay
Nicholas R Leslie
C Peter Downes
Ian H Batty
University of Dundee · GBMRC Protein Phosphorylation and Ubiquitylation Unit · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council G 0801865Medical Research Council G0801865Medical Research Council G9403619Wellcome TrustWellcome Trust 083481
6 · The paper itself

Abstract

Class I phosphoinositide 3-kinases exert important cellular effects through their two primary lipid products, phosphatidylinositol 3,4,5-trisphosphate and phosphatidylinositol 3,4-bisphosphate (PtdIns(3,4)P(2)). As few molecular targets for PtdIns(3,4)P(2) have yet been identified, a screen for PI 3-kinase-responsive proteins that is selective for these is described. This features a tertiary approach incorporating a unique, primary recruitment of target proteins in intact cells to membranes selectively enriched in PtdIns(3,4)P(2). A secondary purification of these proteins, optimized using tandem pleckstrin homology domain containing protein-1 (TAPP-1), an established PtdIns(3,4)P(2) selective ligand, yields a fraction enriched in proteins of potentially similar lipid binding character that are identified by liquid chromatography-tandem MS. Thirdly, this approach is coupled to stable isotope labeling with amino acids in cell culture using differential isotope labeling of cells stimulated in the absence and presence of the PI 3-kinase inhibitor wortmannin. This provides a ratio-metric readout that distinguishes authentically responsive components from copurifying background proteins. Enriched fractions thus obtained from astrocytoma cells revealed a subset of proteins that exhibited ratios indicative of their initial, cellular responsiveness to PI 3-kinase activation. The inclusion among these of tandem pleckstrin homology domain containing protein-1, three isoforms of Akt, switch associated protein-70, early endosome antigen-1 and of additional proteins expressing recognized lipid binding domains demonstrates the utility of this strategy and lends credibility to the novel candidate proteins identified. The latter encompass a broad set of proteins that include the gene product of TBC1D2A, a putative Rab guanine nucleotide triphosphatase activating protein (GAP) and IQ motif containing GAP1, a potential tumor promoter. A sequence comparison of the former protein indicates the presence of a pleckstrin homology domain whose lipid binding character remains to be established. IQ motif containing GAP1 lacks known lipid interacting components and a preliminary analysis here indicates that this may exemplify a novel class of atypical phosphoinositide (aPI) binding domain.

Indexed as

Signal TransductionCell Line, TumorFeasibility StudiesHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsPeptide FragmentsPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesProtein BindingProtein Interaction Domains and MotifsProtein Interaction Mappingras GTPase-Activating ProteinsRecombinant Fusion ProteinsSurface Plasmon ResonanceIntracellular Signaling Peptides and ProteinsIQ motif containing GTPase activating protein 1Membrane ProteinsPeptide FragmentsPhosphatidylinositol 3-KinasesPhosphatidylinositol PhosphatesPLEKHA1 protein, humanras GTPase-Activating ProteinsRecombinant Fusion Proteins

Identifiers

PMID21263009
PMCPMC3069342
OpenAlexW2169229273

What OpenQuestion holds

Textmetadata
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.