Evidence map›Paper›PMID 20497537›Full record

ArticleBMC medical genomics2010

Dynamic cross-talk analysis among TNF-R, TLR-4 and IL-1R signalings in TNFalpha-induced inflammatory responses.

Shih-Kuang Yang, Yu-Chao Wang, Chun-Cheih Chao, Yung-Jen Chuang, Chung-Yu Lan, Bor-Sen Chen

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  12. Anti-Inflammatory Activity of Triterpenes Isolated from Protium paniculatum Oil-Resins.Evidence-based complementary and alternative medicine : eCAM · 2015
    Article
  13. Article
  14. Cucurbitacin E exhibits anti-inflammatory effect in RAW 264.7 cells via suppression of NF-κB nuclear translocation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013
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  20. The influence of tumour necrosis factor- α (TNF-α) on amyloid-β (Aβ)-degrading enzymes in vitro.International journal of molecular epidemiology and genetics · 2011
    Article
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 1 institution in 1 country.

Shih-Kuang YangLaboratory of Control and Systems Biology, Department of Electrical Engineering, National Tsing Hua University, Hsinchu, Taiwan.
Yu-Chao Wang
Chun-Cheih Chao
Yung-Jen Chuang
Chung-Yu Lan
Bor-Sen Chen
National Tsing Hua University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDevelopment in systems biology research has accelerated in recent years, and the reconstructions for molecular networks can provide a global view to enable in-depth investigation on numerous system properties in biology. However, we still lack a systematic approach to reconstruct the dynamic protein-protein association networks at different time stages from high-throughput data to further analyze the possible cross-talks among different signaling/regulatory pathways.

methodsIn this study we integrated protein-protein interactions from different databases to construct the rough protein-protein association networks (PPANs) during TNFalpha-induced inflammation. Next, the gene expression profiles of TNFalpha-induced HUVEC and a stochastic dynamic model were used to rebuild the significant PPANs at different time stages, reflecting the development and progression of endothelium inflammatory responses. A new cross-talk ranking method was used to evaluate the potential core elements in the related signaling pathways of toll-like receptor 4 (TLR-4) as well as receptors for tumor necrosis factor (TNF-R) and interleukin-1 (IL-1R).

resultsThe highly ranked cross-talks which are functionally relevant to the TNFalpha pathway were identified. A bow-tie structure was extracted from these cross-talk pathways, suggesting the robustness of network structure, the coordination of signal transduction and feedback control for efficient inflammatory responses to different stimuli. Further, several characteristics of signal transduction and feedback control were analyzed.

conclusionsA systematic approach based on a stochastic dynamic model is proposed to generate insight into the underlying defense mechanisms of inflammation via the construction of corresponding signaling networks upon specific stimuli. In addition, this systematic approach can be applied to other signaling networks under different conditions in different species. The algorithm and method proposed in this study could expedite prospective systems biology research when better experimental techniques for protein expression detection and microarray data with multiple sampling points become available in the future.

Indexed as

Receptor Cross-TalkDatabases, FactualEndothelial CellsGene Expression ProfilingHumansInflammation MediatorsModels, BiologicalProtein BindingReceptors, Interleukin-1Receptors, Tumor Necrosis FactorSignal TransductionTime FactorsToll-Like Receptor 4Tumor Necrosis Factor-alphaInflammation MediatorsReceptors, Interleukin-1Receptors, Tumor Necrosis FactorToll-Like Receptor 4Tumor Necrosis Factor-alpha

Identifiers

PMID20497537
PMCPMC2889840
OpenAlexW2099566966

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.