Evidence map›Paper›PMID 18055537›Full record

ArticleBiophysical journal2008

SRC family kinases and receptors: analysis of three activation mechanisms by dynamic systems modeling.

Hendrik Fuss, Werner Dubitzky, C Stephen Downes, Mary Jo Kurth

Abstract read
In one paragraph

Article in Biophysical journal, 2008. 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
0.5field-weighted citation impact, top 34% 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, 11 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Hendrik FussSchool of Biomedical Sciences, University of Ulster, Coleraine, Ireland. h.fuss@ulster.ac.uk
Werner Dubitzky
C Stephen Downes
Mary Jo Kurth
University of Ulster · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Src family kinases (SFKs) interact with a number of cellular receptors. They participate in diverse signaling pathways and cellular functions. Most of the receptors involved in SFK signaling are characterized by similar modes of regulation. This computational study discusses a general kinetic model of SFK-receptor interaction. The analysis of the model reveals three major ways of SFK activation: release of inhibition by C-terminal Src kinase, weakening of the inhibitory intramolecular phosphotyrosine-SH2 interaction, and amplification of a stimulating kinase activity. The SFK model was then extended to simulate interaction with growth factor and T-cell receptors. The modular SFK signaling system was shown to adapt to the requirements of specific signaling contexts and yield qualitatively different responses in the different simulated environments. The model also provides a systematic overview of the major interactions between SFKs and various cellular signaling systems and identifies their common properties.

Indexed as

AnimalsBiophysicsComputational BiologyEnzyme ActivationHumansKineticsModels, BiologicalModels, TheoreticalPhosphorylationProtein BindingProtein Structure, TertiaryProtein TransportSignal TransductionSoftwaresrc-Family Kinasessrc-Family Kinases

Identifiers

PMID18055537
PMCPMC2257915
OpenAlexW2100996999

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.