Evidence map›Paper›PMID 22499769›Full record

ArticleMolecular & cellular proteomics : MCP2012

Identification of targets of c-Src tyrosine kinase by chemical complementation and phosphoproteomics.

Isabel Martinez Ferrando, Raghothama Chaerkady, Jun Zhong, Henrik Molina, Harrys K C Jacob, Katie Herbst-Robinson, Beverley M Dancy, Vikram Katju, Ron Bose, Jin Zhang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 62 citations in OpenAlex.

  1. Selective Targeting of Tip Endothelial Cells as a Therapeutic Strategy for Tumor Angiogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  15. How the Discovery of the CD4/CD8-p56Frontiers in cell and developmental biology · 2021
    Review
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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

12 authors at 4 institutions in 2 countries.

Isabel Martinez FerrandoDepartment of Pharmacology and Molecular Sciences, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA.
Raghothama Chaerkady
Jun Zhong
Henrik Molina
Harrys K C Jacob
Katie Herbst-Robinson
Beverley M Dancy
Vikram Katju
Ron Bose
Jin Zhang
Akhilesh Pandey
Philip A Cole
University of Maryland, Baltimore · USJohns Hopkins University · USJohns Hopkins Medicine · USInternational Institute of Information Technology Bangalore · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular proto-oncogene c-Src is a nonreceptor tyrosine kinase involved in cell growth and cytoskeletal regulation. Despite being dysregulated in a variety of human cancers, its precise functions are not fully understood. Identification of the substrates of c-Src remains a major challenge, because there is no simple way to directly stimulate its activity. Here we combine the chemical rescue of mutant c-Src and global quantitative phosphoproteomics to obtain the first high resolution snapshot of the range of tyrosine phosphorylation events that occur in the cell immediately after specific c-Src stimulation. After enrichment by anti-phosphotyrosine antibodies, we identified 29 potential novel c-Src substrate proteins. Tyrosine phosphopeptide mapping allowed the identification of 382 nonredundant tyrosine phosphopeptides on 213 phosphoproteins. Stable isotope labeling of amino acids in cell culture-based quantitation allowed the detection of 97 nonredundant tyrosine phosphopeptides whose level of phosphorylation is increased by c-Src. A large number of previously uncharacterized c-Src putative protein targets and phosphorylation sites are presented here, a majority of which play key roles in signaling and cytoskeletal networks, particularly in cell adhesion. Integrin signaling and focal adhesion kinase signaling pathway are two of the most altered pathways upon c-Src activation through chemical rescue. In this context, our study revealed the temporal connection between c-Src activation and the GTPase Rap1, known to stimulate integrin-dependent adhesion. Chemical rescue of c-Src provided a tool to dissect the spatiotemporal mechanism of activation of the Rap1 guanine exchange factor, C3G, one of the identified potential c-Src substrates that plays a role in focal adhesion signaling. In addition to unveiling the role of c-Src in the cell and, specifically, in the Crk-C3G-Rap1 pathway, these results exemplify a strategy for obtaining a comprehensive understanding of the functions of nonreceptor tyrosine kinases with high specificity and kinetic resolution.

Indexed as

AnimalsBlotting, WesternCSK Tyrosine-Protein KinaseEmbryo, MammalianFibroblastsFocal AdhesionsGuanine Nucleotide-Releasing Factor 2HumansImidazolesMass SpectrometryMiceMice, KnockoutMicroscopy, ConfocalMutationPhosphopeptidesPhosphoproteinsCSK protein, humanCSK Tyrosine-Protein KinaseGuanine Nucleotide-Releasing Factor 2ImidazolesMAS1 protein, humanPhosphopeptidesPhosphoproteinsProto-Oncogene Masrap1 GTP-Binding Proteinssrc-Family KinasesTyrosine

Identifiers

PMID22499769
PMCPMC3412967
OpenAlexW2037820010

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.