Evidence map›Paper›PMID 22851037›Full record

ArticleMolecular bioSystems2012

Robust co-regulation of tyrosine phosphorylation sites on proteins reveals novel protein interactions.

Kristen M Naegle, Forest M White, Douglas A Lauffenburger, Michael B Yaffe

Open access · greenAbstract read
In one paragraph

Article in Molecular bioSystems, 2012. 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
–field-weighted citation impact, top 96% 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, 0 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The unexpected versatility of ALP/Enigma family proteins.Frontiers in cell and developmental biology · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Multidimensional proteomics for cell biology.Nature reviews. Molecular cell biology · 2015
    Review
  12. Article
  13. System level dynamics of post-translational modifications.Current opinion in biotechnology · 2014
    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

4 authors at 1 institution in 1 country.

Kristen M NaegleThe David H. Koch Institute for Integrative Cancer Research, Washington University in St. Louis, St. Louis, MO 63130, USA. knaegle@wustl.edu
Forest M White
Douglas A Lauffenburger
Michael B Yaffe
Washington University in St. Louis · US

Funding

Systems Biology of Cell Decision ProcessesP50GM068762 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 2003 to 2012
$32.3M
Tumor Cell Networks CenterU54CA112967 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI LAUFFENBURGER, DOUGLAS A · 2004 to 2015
$26.2M
Engineered Antibody EGFR Antagonist Cancer TherapeuticsR01CA096504 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI WITTRUP, KARL DANE · 2002 to 2017
$9.7M
Protein Kinase Signaling and Cell Cycle ControlR01ES015339 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 2007 to 2017
$4.3M
NCI NIH HHS R01 CA096504NCI NIH HHS R01-CA96504NCI NIH HHS U54 CA112967NCI NIH HHS U54-CA112967NIEHS NIH HHS R01 ES-015339NIEHS NIH HHS R01 ES015339NIGMS NIH HHS P50 GM068762NIGMS NIH HHS P50-GM68762
6 · The paper itself

Abstract

Cell signaling networks propagate information from extracellular cues via dynamic modulation of protein-protein interactions in a context-dependent manner. Networks based on receptor tyrosine kinases (RTKs), for example, phosphorylate intracellular proteins in response to extracellular ligands, resulting in dynamic protein-protein interactions that drive phenotypic changes. Most commonly used methods for discovering these protein-protein interactions, however, are optimized for detecting stable, longer-lived complexes, rather than the type of transient interactions that are essential components of dynamic signaling networks such as those mediated by RTKs. Substrate phosphorylation downstream of RTK activation modifies substrate activity and induces phospho-specific binding interactions, resulting in the formation of large transient macromolecular signaling complexes. Since protein complex formation should follow the trajectory of events that drive it, we reasoned that mining phosphoproteomic datasets for highly similar dynamic behavior of measured phosphorylation sites on different proteins could be used to predict novel, transient protein-protein interactions that had not been previously identified. We applied this method to explore signaling events downstream of EGFR stimulation. Our computational analysis of robustly co-regulated phosphorylation sites, based on multiple clustering analysis of quantitative time-resolved mass-spectrometry phosphoproteomic data, not only identified known sitewise-specific recruitment of proteins to EGFR, but also predicted novel, a priori interactions. A particularly intriguing prediction of EGFR interaction with the cytoskeleton-associated protein PDLIM1 was verified within cells using co-immunoprecipitation and in situ proximity ligation assays. Our approach thus offers a new way to discover protein-protein interactions in a dynamic context- and phosphorylation site-specific manner.

Indexed as

Chromatography, LiquidData MiningEpithelial CellsErbB ReceptorsFemaleHumansImmunohistochemistryImmunoprecipitationLigandsLIM Domain ProteinsMammary Glands, HumanMicrofilament ProteinsPhosphoproteinsPhosphorylationPrimary Cell CultureProtein BindingEGFR protein, humanErbB ReceptorsLDB2 protein, humanLigandsLIM Domain ProteinsMicrofilament ProteinsPhosphoproteinsTranscription FactorsTyrosine

Identifiers

PMID22851037
PMCPMC3501258
OpenAlexW1533979533

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.