Evidence map›Paper›PMID 25863072›Full record

ArticleBiophysical journal2015

Use of mechanistic models to integrate and analyze multiple proteomic datasets.

Edward C Stites, Meraj Aziz, Matthew S Creamer, Daniel D Von Hoff, Richard G Posner, William S Hlavacek

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2015. 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
1.4field-weighted citation impact, top 19% 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, 24 citations in OpenAlex.

  1. Article
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  12. How low can you go?eLife · 2018
    Article
  13. Article
  14. Article
  15. Mathematics in modern immunology.Interface focus · 2016
    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 4 institutions in 1 country.

Edward C StitesClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona; Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, Missouri. Electronic address: estites@path.wustl.edu.
Meraj AzizClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona.
Matthew S CreamerClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona; Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut.
Daniel D Von HoffClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona.
Richard G PosnerClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona; Department of Biological Sciences, Northern Arizona University, Flagstaff, Arizona. Electronic address: rposner@tgen.org.
William S HlavacekClinical Translational Research Division, Translational Genomics Research Institute, Phoenix, Arizona; Theoretical Biology and Biophysics Group, Theoretical Division, Los Alamos National Laboratory, Los Alamos, New Mexico. Electronic address: wish@lanl.gov.
Translational Genomics Research Institute · USNorthern Arizona University · USWashington University in St. Louis · USYale University · US

Funding

UNM TRAININGP50GM085273 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI LIDKE, KEITH A · 2009 to 2018
$26.1M
Hardening Software for Rule-based models-Competitive RevisionR01GM111510 · NIGMS · NORTHERN ARIZONA UNIVERSITY · PI HLAVACEK, WILLIAM S, POSNER, RICHARD G · 2014 to 2023
$2.8M
NIGMS NIH HHS P50 GM085273NIGMS NIH HHS P50GM085273NIGMS NIH HHS R01 GM111510NIGMS NIH HHS R01GM111510
6 · The paper itself

Abstract

Proteins in cell signaling networks tend to interact promiscuously through low-affinity interactions. Consequently, evaluating the physiological importance of mapped interactions can be difficult. Attempts to do so have tended to focus on single, measurable physicochemical factors, such as affinity or abundance. For example, interaction importance has been assessed on the basis of the relative affinities of binding partners for a protein of interest, such as a receptor. However, multiple factors can be expected to simultaneously influence the recruitment of proteins to a receptor (and the potential of these proteins to contribute to receptor signaling), including affinity, abundance, and competition, which is a network property. Here, we demonstrate that measurements of protein copy numbers and binding affinities can be integrated within the framework of a mechanistic, computational model that accounts for mass action and competition. We use cell line-specific models to rank the relative importance of protein-protein interactions in the epidermal growth factor receptor (EGFR) signaling network for 11 different cell lines. Each model accounts for experimentally characterized interactions of six autophosphorylation sites in EGFR with proteins containing a Src homology 2 and/or phosphotyrosine-binding domain. We measure importance as the predicted maximal extent of recruitment of a protein to EGFR following ligand-stimulated activation of EGFR signaling. We find that interactions ranked highly by this metric include experimentally detected interactions. Proteins with high importance rank in multiple cell lines include proteins with recognized, well-characterized roles in EGFR signaling, such as GRB2 and SHC1, as well as a protein with a less well-defined role, YES1. Our results reveal potential cell line-specific differences in recruitment.

Indexed as

Datasets as TopicModels, BiologicalSignal TransductionAnimalsErbB ReceptorsHeLa CellsHumansProteomeShc Signaling Adaptor Proteinssrc Homology DomainsErbB ReceptorsProteomeShc Signaling Adaptor Proteins

Identifiers

PMID25863072
PMCPMC4390817
OpenAlexW2092133543

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.