Evidence map›Paper›PMID 26503892›Full record

ArticleMolecular & cellular proteomics : MCP2015

Temporal Phosphoproteome Dynamics Induced by an ATP Synthase Inhibitor Citreoviridin.

Chia-Wei Hu, Chia-Lang Hsu, Yu-Chao Wang, Yasushi Ishihama, Wei-Chi Ku, Hsuan-Cheng Huang, Hsueh-Fen Juan

Open access · hybridAbstract read
In one paragraph

Article in Molecular & cellular proteomics : MCP, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. Review
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  9. Article
  10. Quantitative proteomics in lung cancer.Journal of biomedical science · 2017
    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

7 authors at 5 institutions in 2 countries.

Chia-Wei HuFrom the ‡Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan;
Chia-Lang Hsu§Department of Life Science, National Taiwan University, Taipei 106, Taiwan;
Yu-Chao Wang¶Institute of Biomedical Informatics, Center for Systems and Synthetic Biology, National Yang-Ming University, Taipei 112, Taiwan;
Yasushi Ishihama‖Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto 606-8501, Japan;
Wei-Chi Ku**School of Medicine, Fu Jen Catholic University, New Taipei City 242, Taiwan;
Hsuan-Cheng Huang¶Institute of Biomedical Informatics, Center for Systems and Synthetic Biology, National Yang-Ming University, Taipei 112, Taiwan; hsuancheng@ym.edu.tw yukijuan@ntu.edu.tw.
Hsueh-Fen JuanFrom the ‡Institute of Molecular and Cellular Biology, National Taiwan University, Taipei 106, Taiwan; §Department of Life Science, National Taiwan University, Taipei 106, Taiwan; ‡‡Genome and Systems Biology Degree Program, National Taiwan University, Taipei 106, Taiwan; §§Graduate Institute of Biomedical Electronics and Bioinformatics, National Taiwan University, Taipei 106, Taiwan hsuancheng@ym.edu.tw yukijuan@ntu.edu.tw.
National Taiwan University · TWFu Jen Catholic University · TWKyoto Pharmaceutical University · JPNational Center for Theoretical Sciences · TWNational Yang Ming Chiao Tung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Citreoviridin, one of toxic mycotoxins derived from fungal species, can suppress lung cancer cell growth by inhibiting the activity of ectopic ATP synthase, but has limited effect on normal cells. However, the mechanism of citreoviridin triggering dynamic molecular responses in cancer cells remains unclear. Here, we performed temporal phosphoproteomics to elucidate the dynamic changes after citreoviridin treatment in cells and xenograft model. We identified a total of 829 phosphoproteins and demonstrated that citreoviridin treatment affects protein folding, cell cycle, and cytoskeleton function. Furthermore, response network constructed by mathematical modeling shows the relationship between the phosphorylated heat shock protein 90 β and mitogen-activated protein kinase signaling pathway. This work describes that citreoviridin suppresses cancer cell growth and mitogen-activated protein kinase/extracellular signal-regulated kinase signaling by site-specific dephosphorylation of HSP90AB1 on Serine 255 and provides perspectives in cancer therapeutic strategies.

Indexed as

AnimalsAurovertinsCell CycleCell Line, TumorEnzyme InhibitorsGene Expression Regulation, NeoplasticHSP90 Heat-Shock ProteinsHumansLung NeoplasmsMAP Kinase Signaling SystemMiceModels, TheoreticalPhosphorylationProtein FoldingProteomeXenograft Model Antitumor AssaysAurovertinscitreoviridinEnzyme InhibitorsHSP90AB1 protein, humanHSP90 Heat-Shock ProteinsProteome

Identifiers

PMID26503892
PMCPMC4762618
OpenAlexW2175830459

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.